Early Life Nutrition and Lifelong Health PDF

BMA Board of Science
Early life nutrition and

lifelong health
February 2009
Early life nutrition and

lifelong health
February 2009
Early life nutrition and lifelong health i

Editorial board
A publication from the BMA Science and Education department and the Board of Science.
Chair, Board of Science Professor Sir Charles George
Director of Professional Activities Professor Vivienne Nathanson
Head of Science and Education/Project lead Nicky Jayesinghe
Authors Professor Mark Hanson

Professor Caroline Fall
Dr Sian Robinson
Dr Janis Baird
Contributors Luke Garland

Dr Joseph Kirkman (PhD)
Dr Caroline Seddon (PhD)
Editorial secretariat Thom Ellinas

Hilary Forrester
Darshna Gohil
Dr Madelaine Healey (PhD)
David Maynard
Sarah Mills
George Roycroft
Indexer Richard Jones
British Library Cataloguing-in-Publication Data.

A catalogue record for this book is available from the British Library.
ISBN: 978-1-905545-32-2
Cover photograph: Getty Images
British Medical Association 2009 all rights reserved. No part of this publication may be
reproduced, stored in a retrievable system or transmitted in any form or by any other means that
be electrical, mechanical, photocopying, recording or otherwise, without the prior permission in
writing of the British Medical Association.
ii Early life nutrition and lifelong health

Board of Science
This report was prepared under the auspices of the Board of Science of the British Medical Association,
whose membership for 2008/09 was as follows:
Sir Kenneth Calman President, BMA

Dr Peter Bennie Chair of the Representative Body, BMA
Dr Hamish Meldrum Chair of Council
Dr David Pickersgill Treasurer, BMA
Mr Tony Bourne Chief Executive, BMA
Dr Kate Bullen Deputy Chair of Council
Professor Sir Charles George Chair, Board of Science
Dr Andrew Thomson Deputy Chair, Board of Science
Dr Mohammad Anwar
Dr JS Bamrah
Mr Philip Belcher
Dr Andrew Collier
Dr Peter Dangerfield
Dr Lucy-Jane Davis
Dr Peter Maguire
Dr David Sinclair
Dr Dorothy Ward
Dr David Wrigley
Dr Richard Jarvis (by invitation)
Professor Parveen Kumar (Co-optee)
Dr Philip Steadman (Co-optee)
Dr Ram Moorthy (Deputy member)
Approval for publication as a BMA policy report was recommended by BMA Board of Professional
Activities on 14 July 2008.
Declaration of interest
There were no competing interests with anyone involved in the research and writing of this
report. For further information about the editorial secretariat or Board members please contact
the Science and Education Department which holds a record of all declarations of interest:
info.science@bma.org.uk
Early life nutrition and lifelong health iii

Acknowledgements
The Association is grateful for the help provided by the BMA committees and outside experts and
organisations. We would particularly like to thank:
Professor Mark Hanson, Director Institute of Developmental Sciences, Director Developmental

Origins of Health and Disease Division, British Heart Foundation Professor of Cardiovascular Science,
University of Southampton
Professor Caroline Fall, Professor of International Paediatric Epidemiology, Medical Research Council
(MRC) Epidemiology Resource Centre, University of Southampton
Dr Sian Robinson, Principal Research Fellow, MRC Epidemiology Resource Centre, University of
Southampton
Dr Janis Baird, Senior Research Fellow and Honorary Consultant in Public Health, MRC Epidemiology
Resource Centre, University of Southampton
Professor Alan Jackson, Director, Institute of Human Nutrition, Developmental Origins of Health and
Disease Division, University of Southampton
Professor Cyrus Cooper, Director of the MRC Epidemiology Resource Centre and Professor of
Rheumatology at the University of Southampton
Professor Keith Godfrey, MRC Epidemiology Resource Centre, University of Southampton and
Centre for Developmental Origins of Health and Disease, University of Southampton
Dr Tim Lobstein, Director of the Childhood Obesity Programme International Association for the
Study of Obesity.
Parts of the report are based on reviews by Professor Mark Hanson with Professors Gluckman or
Poston. The authors are grateful to Mrs Jane Kitcher for preparation of the manuscript.
Address for correspondence: Professor Mark Hanson, Institute of Developmental Sciences,

Mailpoint 887, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD
Tel: 02380 798421 Fax: 02380 795255 Email: m.hanson@soton.ac.uk
iv Early life nutrition and lifelong health

About the authors
Mark Hanson MA DPhil Cert Ed FRCOG is Director of the Division of Developmental Origins of Health
and Disease and British Heart Foundation Professor of Cardiovascular Science at the University
of Southampton School of Medicine. He is founding Director of the Institute of Developmental
Sciences at Southampton. His research concerns the ways in which the developmental
environment, and especially nutrition, affects cardiovascular, metabolic and behavioural
characteristics of the individual, influencing how well they respond to later challenges and
the resulting risks of disease. He is much involved in promoting the public understanding of this
area of biomedical science.
Caroline Fall MBChB, DM, FRCP, FRCPCH is a consultant paediatrician and Professor of International
Paediatric Epidemiology at the MRC Epidemiology Resource Centre, University of Southampton.
Her research focuses on the effects of maternal and infant nutrition on obesity, diabetes and
cardiovascular disease in later life.
Sian Robinson PhD R Nutr is a Registered Nutritionist and a Principal Research Fellow at the
MRC Epidemiology Resource Centre at the University of Southampton. She is responsible for
the nutritional components of two large UK cohorts run by the Epidemiology Resource Centre,
the Southampton Womens Survey and the Hertfordshire Cohort Study. Her principal research
interests are in maternal and infant nutrition.
Janis Baird MB BCh, PhD, FFPH is a Senior Research Fellow and Honorary Consultant in Public Health
at the MRC Epidemiology Resource Centre, University of Southampton. Her research focuses on
translating evidence of the developmental origins of health and disease into public health policy.
Early life nutrition and lifelong health v

Abbreviations
AA Arachidonic acid
AGA Appropriate-for-gestational-age
ALSPAC Avon Longitudinal Study of Parents and Children
ARM Annual representative meeting
BMA British Medical Association
BMC Bone mineral content
BMI Body mass index
CHD Coronary heart disease
CI Confidence intervals
COMA Committee on Medical Aspects of Food and Nutrition
CSE Certificate of secondary education
DALY Disability adjusted life year
DDT Dichlorodiphenyl trichloroethane
DH Department of Health
DHA Docosahexanoic acid
DNA Deoxyribonucleic acid
Dnmt DNA N-methyl transferase
DXA Dual-energy x-ray absorptiometry
EFNEP Expanded Food and Nutrition Education Programme
FSA Food Standards Agency
GP General practitioner
HDL High-density lipoprotein
HIV Human Immunodeficiency Virus
IBFAN International Baby Food Action Network
IFS Infant feeding survey
Ig Immunoglobulin
IGF Insulin-like growth factors
IGT Impaired glucose tolerance
INCAP Institute of Nutrition of Central American and Panama
IQ Intelligence quotient
IUGR Intrauterine growth restriction
LCPUFA Long-chain polyunsaturated fatty acids
LDL Low-density lipoprotein
LGA Large-for-gestational-age
LIDNS Low Income Diet and Nutrition Survey
MRC Medical Research Council
NDNS National Diet and Nutrition Survey
NICE National Institute for Health and Clinical Excellence
PCB Polychlorinated biphenyls
PSA Public service agreement
RB Representative body
RCPCH Royal College of Paediatrics and Child Heath
RCT Randomised controlled trial
SACN Scientific Advisory Committee on Nutrition
SBP Systolic blood pressure
SD Standard deviation
SGA Small-for-gestational-age
UK United Kingdom
UNICEF United Nations Childrens Fund
USA United States of America
WHO World Health Organisation
WIC US Special Supplemental Nutrition Programme for Women, Infants and Children
vi Early life nutrition and lifelong health

Glossary
Adiposity relating to, or composed of adipose tissue containing fat cells

Anaemia a condition in which the number of active red blood cells and/or levels of the oxygen
carrying pigment haemoglobin in the blood is reduced
Atherogenic conducive to or causing atherogenesis, or the build up of fatty deposits in the arteries,
which leads to cardiovascular disease
Body mass index an indicator of whether a person is under- or overweight, derived from the
weight of a person (in kilograms) divided by the square of their height (in metres)
Cardiomyocytes cardiac muscle cells
Cardiovascular disease all conditions that affect the heart and blood vessels
Coeliac disease a condition in which the small intestine fails to digest and absorb food, due to a
permanent sensitivity to the protein gliadin, contained in gluten
Coronary heart disease heart disease caused by narrowing of the arteries that supply blood to the
heart
Diastolic blood pressure the pressure of the blood against the walls of the main arteries when the
ventricles are relaxed and refilling
Disability adjusted life year (DALY) a health gap measure that extends the concept of potential
years of life lost due to premature death to include equivalent years of healthy life lost by virtue of
being in states of poor health or disability
Dual-energy X-ray absorptiometry a means of measuring bone mineral density
Dyslipidaemia a disturbance in the amount of lipid in the blood
Epigenetic please refer to Appendix 1
FTO gene a gene on chromosome 16 in humans, certain variants of which appear to correlate with
obesity in humans
Galactosaemia the inability to utilise the sugar galactose, leading to its accumulation within the
blood
Gastroenteritis the inflammation of the stomach and intestine, usually due to infection or food-
poisoning
Gastro-intestinal illness illness relating to the stomach and the intestine
Glycaemic index a dietary index that is used to rank carbohydrate-based foods. The index indicates
the rate at which the food we eat will increase blood sugar levels
Goitre swelling of the neck due to enlargement of the thyroid gland. This may be due to a lack of
dietary iodine
Gonadotrophin any of several hormones synthesised and released by the pituitary gland that act on
the testes or ovaries to promote the production of sex hormones and either sperm or ova
Hodgkins lymphoma a malignant disease of lymphatic tissue, usually characterised by painless
enlargement of one or more groups of lymph nodes
Homeostasis the physiological process by which the internal systems of the body are maintained at
equilibrium, despite variations in external conditions
Hyperinsulinaemia excessive insulin secretion
Hyperphagia abnormally large intake of food
Hypertension high blood pressure, above the normal range expected for a particular age group
and sex
In utero a Latin term meaning inside the womb, and used with reference to the fetus during
pregnancy
Insulin-like growth factors polypeptides with high sequence similarity to insulin, they are part of a
complex system that cells use to communicate with their physiological environment and to regulate
their growth and metabolism
Intrauterine growth restriction a reduction in the growth of the fetus, most commonly resulting
from placental dysfunction, poor maternal nutrition, or maternal smoking, and resulting in a baby that
is small for gestational age.
Early life nutrition and lifelong health vii

Ischaemic heart disease heart disease resulting from an inadequate flow of blood to the heart,
caused by narrowing or blockage of the blood vessels supplying it
Lymphoblastic leukaemia a type of leukaemia characterised by abnormal cells with a large nucleus
and little cytoplasm present in the blood and blood forming organs
Mastitis inflammation of the breast, usually caused by bacterial infection via damaged nipples
Meiosis a type of cell division, consisting of two successive separations, resulting in four daughter
cells, each with half the original number of chromosomes of the original cell; the process used in
gamete (sperm and ova) formation
Meiotic pertaining to meiosis
Mitosis a type of cell division resulting in two daughter cells, genetically identical to the original cell;
the process used in growth
Mitotic pertaining to mitosis
Neuroblastoma a malignant tumour usually of childhood, composed of embryonic nerve cells.
It may originate in any part of the sympathetic nervous system
Non-genomic inheritance any pattern of inheritance in which traits do not segregate in
accordance with genomic factors
Normoglycaemic a condition of the blood in which the blood sugar level is within normal limits
Obesity refer to Appendix 2
Obesogenic factors tending to cause or produce obesity in an individual
Osteoporosis the loss of bone tissue, resulting in bones which are brittle and liable to fracture
Otitis media inflammation of the middle ear associated with perforations of the eardrum
Overweight refer to Appendix 2
Palaeolithic pertaining to a prehistoric era distinguished by the development of the first stone tools,
extending from approximately 2.5 million to around 10,000 years ago
Perinatal care care relating to the period starting a few weeks before birth, including birth and a
few weeks after birth
Phenotype the observable characteristics of an individual resulting from the interaction between
their genes and the environment
Plasminogen activator inhibitor an inhibitor of enzymes that convert inactive plasminogen into
the active enzyme plasmin, which digests blood clots
Polymorphism a condition in which a chromosome or a genetic character occurs in more than one
form, resulting in the coexistence of more than one morphological type within a population
Pro-inflammatory cytokines proteins produced predominantly by activated immune cells, involved
in the amplification of inflammatory reactions
Rickets a disease in which bones do not harden due to a deficiency of vitamin D
Statin any one of a class of pharmaceuticals that inhibit the action of an enzyme
(hydroxymethylglutaryl coenzyme A reductase) involved in the production of cholesterol within the liver
Stroke a sudden attack of weakness affecting one side of the body or other loss of neural function
lasting at least 24 hours. It is the consequence of an interruption to the flow of blood to the brain
Systolic blood pressure the pressure of the blood against the walls of the main arteries when the
ventricles are contracting
Teratogenic the effect of a substance, agent or process that induces the formation of
developmental abnormalities in a fetus
Type 1 diabetes an autoimmune disease that results in the permanent destruction of insulin
producing beta cells of the pancreas
Type 2 diabetes a metabolic disorder, primarily characterised by insulin resistance, relative insulin
deficiency and hyperglycaemia
Undernutrition inadequate nutrition from any cause
von Willebrand factor a glycoprotein necessary for platelet function, abnormalities of which can
result in an inherited disorder of the blood which is characterised by episodes of spontaneous bleeding
similar to haemophilia
viii Early life nutrition and lifelong health

Foreword
For 175 years the BMA has promoted medicine and the allied sciences as part of its founding principle
to maintain the honour and interests of the medical profession. One element of this work is to be
advocates for the health of the public. In doing so we listen first to our members concerns. At the
annual representative meeting (ARM) members tell us of the problems they see in the communities
and patients they serve. Motions are proposed by grass roots doctors and debated at the ARM.
Approximately 600 doctors form the representative body (RB), which is the democratically elected,
policy-making body of the BMA. Motions passed at the ARM are usually adopted as BMA policy. A list
of all BMA polices can be found at www.bma.org.uk
This report was commissioned after an ARM debate in June 2007 that called on the BMAs Board of
Science to recognise and promote the importance of fetal and early life nutrition and its relationship to
lifelong health. The Board of Science has previously produced three reports that broadly cover
childhood nutrition and exercise. Growing up in Britain: ensuring a healthy future for our children
(1999) discusses child health, with a focus on nutrition rather than exercise, from conception to the
age of five. Adolescent health (2003) reviews nutrition, exercise and obesity in teenagers (13-19 year
olds). It serves in part to develop the 1999 report in order to cover children up to the age of 12 years.
It highlights the main aspects of childhood nutrition and exercise, draws attention to the role of the
clinician, and provides links to sources of further information. It also makes recommendations for
tackling the obesity epidemic in the UK. Preventing childhood obesity (2005) highlights the situation
with regard to childhood obesity and the impact this can have on childrens current and future health.
It examines the role of healthcare professionals and the environmental barriers to change that need to
be overcome or removed.
This report concerns early life nutrition predominantly fetal and infant nutrition providing useful
reference information and key messages for healthcare professionals. It discusses the evidence-base
and draws conclusions about the ways in which the patterns of early life nutrition can be improved,
and the likely consequences of such improvements. This is now of critical importance in addressing the
rapid increase in the incidence of so-called lifestyle diseases such as cardiovascular disease and type 2
diabetes, which are linked to overweight and obesity. In addition there is now compelling evidence for
a role of early life nutrition in setting the risk of other conditions including osteoporosis, asthma, lung
1
disease and some forms of cancer. Evidence is growing that early life nutrition can play a role in
behavioural and cognitive problems in children and adolescents, and possibly even in cognitive decline
and other aspects of ageing.
This report from the BMA Board of Science is intended to be a useful point of reference for a wide
audience, including health professionals, policy makers and members of the public. The approach of
the BMA Board of Science is to provide a clear synthesis of the available research, and to develop
evidence-based conclusions and recommendations for policy.
Professor Sir Charles George

Chair, Board of Science
The Board of Science, a standing committee of the BMA, provides an interface between the medical profession, the
Government and the public. The Board produces numerous reports containing policies for national action by Government
and other organisations, with specific recommendations affecting the medical and allied professions.
Early life nutrition and lifelong health ix

x Early life nutrition and lifelong health

Contents
Abbreviations vi
Glossary vii
Foreword ix
List of figures xiii
Executive summary 1
Report conclusions 3
Chapter 1: The importance of fetal and infant nutrition 5

Nutritional transitions and patterns of chronic disease 5
What is good nutrition? 7
The developmental consequences of inappropriate nutrition 7
The importance of development for later health 8
Obesity 11
Previous work by the BMA 13
Conclusions 14
Chapter 2: Fetal nutrition: impact on development and later life 15

Impact of fetal nutrition on health in later life: the developmental
origins concept 15
Mechanisms by which fetal nutrition affects risk of later disease 19
Epigenetic mechanisms 20
Maternal undernutrition and long-term outcomes in the offspring 21
Associations between maternal obesity, diabetes, raised birth weight
and adulthood disease 22
Transgenerational effects 22
Conclusions 24
Chapter 3: Infant nutrition 25

Introduction 25
The case for breastfeeding 26
Current infant feeding practices 27
Complementary feeding practices in the UK
Guidelines on infant feeding 34
Breastfeeding guidelines
Maternal diet during lactation guidelines
Formula feeding
Complementary feeding
Vitamin supplements for infants
Determinants of infant weight gain and growth 36
Recommendations about size and growth during infancy
Early life nutrition and lifelong health xi

Breastfeeding and health: short- and long-term outcomes 40

Breastfeeding and later cognitive function and neurodevelopment
Breastfeeding and later body composition and obesity
Diabetes
Blood pressure and cardiovascular disease
Other cardiovascular risk factors
Cancer
Allergic/atopic disease
Mental health
Other outcomes: bone health, coeliac disease, inflammatory bowel disease
Other aspects of infant diet and long-term outcomes 44
The timing of introduction of solids and later health
Infant growth and long-term outcomes
Conclusions 49
Chapter 4: Influences on maternal and infant nutrition and

opportunities for intervention 50
Interventions in maternal and infant nutrition a global perspective 50
Interventions designed to improve short-term outcomes
Guidelines for improving the diets of young women in the UK 51
Influences on food choices in women 53
Interventions to improve maternal nutrition 55
Improving breastfeeding initiation and increasing duration
of breastfeeding 56
The WHO/UNICEF Baby Friendly Hospital Initiative
Doctors role in supporting breastfeeding
NICE Guidance on Breastfeeding
Support for breastfeeding mothers returning to work
Interventions in complementary feeding 61
Mechanisms to address nutritional inequalities in the UK 61
NICE guidance
Healthy Start schemes
Tackling the problem of obesity 63
Conclusions 65
Appendix 1: Epigenetic processes 66
Appendix 2: Definition of overweight 68
Appendix 3: Current UK dietary recommendations for pregnancy 69
Appendix 4: Infant feeding guidelines 71
Appendix 5: The International Code on the Marketing of Breast Milk Substitutes 74
Appendix 6: Comparison of the nutrient composition of mature

human breast milk and formula 75
References 77
INDEX 93
xii Early life nutrition and lifelong health

List of figures
Figure 1: The human dietary transition 6

Figure 2: The thrifty phenotype hypothesis 9
Figure 3: Mismatch model of chronic disease 10
Figure 4: Patterns of infant and childhood growth associated with
later heart disease 17
Figure 5: Graded effects of nutrition in development on later function 18
Figure 6: The fetal supply line for nutrients 19
Figure 7: Cycles of disease risk 23
Figure 8: Prevalence of breastfeeding according to mothers socio-economic
classification: Infant Feeding Survey 2005 30
Figure 9: Age by which solids had been introduced according to mothers
socio-economic classification: Infant Feeding Survey 2005 31
Figure 10: 12-month infant guidelines pattern score according to
prudent diet score of the mother 33
Figure 11: Mean weight and length of breastfed and formula-fed infants
from birth to 18 months 37
Figure 12: Cardiovascular disease mortality according to weight at one year
in Hertfordshire men 46
Figure 13a and 13b: Height and weight scores in infancy of individuals having
CHD in later life 47
Figure 14: Percentage of women with prudent diet scores in lowest quarter of
distribution, according to their educational attainment:
6,125 women in the Southampton Womens Survey 53
Figure 15: Components of the epigenetic code 66
Early life nutrition and lifelong health xiii

xiv Early life nutrition and lifelong health

Executive summary
Studies of human populations show clear links between variability in early life environment and risk
of later ill health and chronic disease. A critical aspect of environment is the interaction of nutrition
with other stressors. Nutrition is important in terms of its quantity and also in the balance of foods
and their components, both macronutrients and micronutrients such as minerals and vitamins. An
inadequate or unbalanced dietary intake can lead to malnutrition: the consequences of which
embrace the range from under-weight, through the normal range to overweight. The health and
other consequences of malnutrition across the entire spectrum are cause for considerable concern
in all societies, especially among the poor and most economically deprived. The risk for this burden
of ill health is set in train from very early life, providing opportunities for effective interventions at
all ages. Future research will help identify further opportunities for effective interventions through
better definition of biomarkers of risk, and underlying mechanisms.
In developed societies many women consume poor quality diets, which may result in nutritional
deficiencies on the one hand and overweight and obesity on the other. In developing societies
maternal under-nutrition remains a major problem but maternal overweight is also of concern.
Effective interventions are therefore needed to improve the nutrition of young women of childbearing
age in many societies. Less healthy diets are more common among women of low educational
attainment, and among women who have low incomes and who are food insecure. Both nutrition
education and counselling have been shown to improve womens nutrition knowledge and
behaviour. These approaches need to be increased to be effective at a population level and other
interventions developed to improve the diets of young women as a matter of urgency.
Our understanding of the specific mechanisms through which maternal nutrition leads to long-
term effects is limited in humans, but there is strong evidence relevant to human disease from
studies in animals that changing nutrition in pregnancy can produce effects on the offspring.
Underlying mechanisms use developmental plasticity to produce adaptive responses to nutritional
cues crossing the placenta from the mother. Some cues may even operate in the periconceptional
period, before the woman knows she is pregnant. Positive steps therefore need to be taken to
ensure that young people understand the importance of health and well-being before pregnancy
giving attention to their diet, maintaining a healthy body weight, stopping smoking and limiting
alcohol consumption.
Infants are particularly vulnerable because of their immaturity and the nutritional demands of rapid
growth and development. Exclusive breastfeeding is recommended for at least the first six months
of life and is associated with reduced susceptibility to infection. The preferred growth associated
with breastfeeding enables normal cognitive and physical development and may protect against
obesity and chronic disease in adult life. Breastfeeding rates are unacceptably low in the UK and
especially so among disadvantaged women. Mothers may need personal support to establish
successful breastfeeding and wider society should support parents in the initiation and
prolongation of the duration of breastfeeding. Interventions which educate women about the
benefits and practice of breastfeeding, and which promote baby friendly policy and practice, are
effective at promoting the initiation and prolonging the duration of breastfeeding. The ten steps to
successful breastfeeding and the Baby Friendly Hospital Initiative guidelines should become a
minimum standard of care. Action is also needed to improve the opportunities for women to
breastfeed in public places and to support women who return to work to continue breastfeeding.
There are wide variations in complementary feeding [weaning] practice in the UK. The influence of
the timing and nutritional content of complementary feeding and the specific effects of variations
in quality of complementary feeding on current and later health in countries such as the UK are
still to be determined. There are wide variations in infant size, weight gain, linear growth and body
Early life nutrition and lifelong health 1

composition. There is increasing evidence that these influence the risk of developing obesity,
diabetes, cardiovascular disease and other health outcomes in later life. The optimal pattern(s) of
infant growth to minimise the risk of obesity, cardiovascular disease and diabetes need(s) to be
determined. There is strong evidence that undernutrition (stunting or wasting) during the first two
years of life leads to impaired adult cognitive, physical and economic capacity, which cannot be
repaired even if nutrition improves later in childhood.
Dietary patterns run in families and the diet of infants tends to be similar to that of mothers. It is
likely that interventions which improve the diets of young women will also lead to improved diets
for their children. The Healthy Start scheme provides support for eligible women and children
through provision of food vouchers and vitamin supplements, and needs to be promoted widely.
Its impact on the nutrition of mothers and young children should be evaluated at a national level.
Development of future interventions highlights the need for biomarkers of poor developmental
nutrition in infants and children.
While there are gaps in the evidence about the long-term consequences of poor maternal and
infant nutrition, and we do not as yet understand the mechanisms fully, it is clear that steps need
to be taken to promote healthy diets in young women and their families, to encourage
breastfeeding and the use of appropriate complementary foods.
2 Early life nutrition and lifelong health

Report conclusions
Chapter 1
Balanced nutrition during human development is of critical importance for later health and
wellbeing and for reducing the risks of many chronic diseases.
Unbalanced nutrition can result from diets which have either excessive or inadequate nutrient
intakes. Energy dense diets can none the less be poor in micronutrients.
The consequences of unbalanced nutrition at both ends of the dietary range are associated with
increased risks of adult chronic disease.
Humans evolved to consume a diet very different from that consumed by many people today.
This makes our physiology potentially mismatched to our contemporary lifestyles, increasing the
risks of ill health.
During development, humans like other animals attempt to match the structure and functions of
their organs and tissues to the world in which they expect to live. The prediction is based on
cues from the mothers environment via the placenta and her milk.
Inaccurate predictions, for example through socio-economic change leading to a nutritional
transition between generations, increase mismatch and risk of disease.
In addition to maternal undernutrition, the rising incidence of maternal obesity and diabetes in
pregnancy will exacerbate the epidemic of chronic disease in developed societies.
As low income countries develop, the cycle of diseases such as diabetes and obesity triggered by
nutritional mismatch may be followed by further cycles arising from relative overnutrition during
fetal and infant development.
Chapter 2
Studies of human populations show clear links between early life environment and later health
and disease.
While our knowledge of the specific components of maternal nutrition which produce such
effects is limited in humans, experimental animal studies provide strong evidence that changing
nutrition in the periconceptional period or in pregnancy can produce effects on the offspring
which mimic human chronic disease.
In developed societies, we know that many women consume poor quality diets, which result on
the one hand in nutritional deficiencies and on the other in overweight and obesity.
In developing societies, while maternal undernutrition remains a major problem, maternal
overweight is also of concern.
Development of future interventions will require the identification of biomarkers of poor
developmental nutrition in infants and children.
There is a need for better understanding of the implications of current variations in diet and
nutrition for fetal development and long-term health.
Positive steps need to be taken to ensure that young people understand the importance of
health and wellbeing before pregnancy giving attention to their diet, optimal body weight, to
stopping smoking and to limiting alcohol consumption.
Chapter 3
Infants have special nutritional requirements because of their rapid growth and development and
vulnerability to infection. Optimal nutrition in infancy is essential for normal cognitive and physical
development and may protect against obesity and chronic disease in adult life. Many parents need
guidance to provide adequate nutrition for their children at this stage of life.
Breast milk is the ideal food for babies in their first few months. Mothers need support in order to
breastfeed successfully. There is consistent evidence of better childhood cognitive development,
and a lower risk of several disease outcomes including obesity and diabetes, in children and adults
who were breastfed rather than formula-fed. It is not known whether these effects are causal or
reflect the generally healthier lifestyles of the families whose mothers choose to breastfeed.

The effects of the quality of complementary feeding on current and later health in countries
such as the UK are largely unknown. There are wide variations in infant size, weight gain, linear
growth and body composition. There is increasing evidence that these influence the risk of
developing obesity, diabetes, cardiovascular disease and other health outcomes in later life. The
optimal pattern(s) of infant weight gain in order to minimise the risk of obesity, cardiovascular
disease and diabetes is, however, not yet known. There is strong evidence that undernutrition
(stunting or wasting) during infancy leads to impaired adult cognitive, physical and economic
capacity, even if nutrition improves later in childhood.
Chapter 4
Many young women have diets of poor quality and inadequate nutritional status. Less healthy
diets are more common among women of low educational attainment, and among women who
have low incomes and who are food insecure. Although evidence of effective interventions to
improve the diets of young women is limited, this does not mean that the goal should not be
pursued vigorously. Both nutrition education and counselling have been shown to improve
womens nutrition knowledge and behaviour.
Breastfeeding rates are low in the UK, and it is less common among disadvantaged women.
Interventions that educate women about the benefits and practice of breastfeeding, and that
promote baby friendly policies and practice, are effective at promoting the initiation and
prolonging the duration of breastfeeding.
Current studies of complementary feeding [weaning] show wide variations in practice in the UK.
There are few studies of interventions to influence the timing and nutritional content of
complementary feeding in developed countries.
Infant diet is strongly linked to mothers diet suggesting that interventions to improve the diets
of young women will also have direct consequences for childrens diets.
Effective interventions are needed to improve the nutrition of young women of childbearing age.
Such interventions may influence the way in which mothers feed their children as well as
influencing the diets of women themselves. They will therefore have beneficial health effects
across generations.
Efforts to encourage the initiation and to prolong the duration of breastfeeding need to continue
and be extended. The ten steps to successful breastfeeding and the Baby Friendly Hospital
Initiative guidelines should become a minimum standard of care. Action is also needed to improve
the opportunities for women to breastfeed in public places and to support continued
breastfeeding in women who return to work.
The Healthy Start scheme provides support for eligible women and children through provision of
food vouchers and vitamin supplements, and needs to be promoted widely. Its impact on the
nutrition of mothers and young children should be evaluated at a national level.
Other gaps in the evidence should be addressed, including interventions to support
breastfeeding mothers in the workplace and interventions to optimise the timing and content of
complementary feeding.

Chapter 1: The importance of fetal

and infant nutrition
Our current level of interest in the link between nutrition and health is unprecedented. Over the
past century nutritional science has grown from the recognition of the properties of nutrients and
their ability to prevent deficiency diseases to an understanding of the benefits of good nutrition
which include the promotion and maintenance of good health and protection from disease. The
definition of an optimal diet which provides a balanced supply of nutrients in sufficient amounts
to support optimal metabolic function is not necessarily clear. What constitutes an appropriate
balance of foods and nutrients in the diet may differ between individuals, based on their genetic
makeup and previous experience.
A poor, unbalanced diet has been shown in recent studies to be common in the general
2
population even in developed societies. Poor micronutrient and vitamin status, such as folate and
vitamin D, occurs in many people but particularly in those of reproductive age even though their
energy intakes may be sufficient. In developing countries maternal and child undernutrition is the
cause of 3.5 million deaths each year, constituting 35 per cent of the burden of disease in children
3
under five years. Sub-optimal breastfeeding, especially non-exclusive breastfeeding in the first six
months of life, results in 1.4 million deaths and 10 per cent of the disease burden in children
3
under five years. At the same time, there are over 300 million people around the world who are
4
obese. The effects of overnutrition are not only a concern in developed societies, living a
Western lifestyle. Populations which are emerging from poverty are also at risk of the adverse
effects on health caused by excesses in the diet, even in people who are not obese by Western
standards. Diets which lead to over-nutrition (eg excess calories) are often micronutrient poor. Thus
the possible effects of poor, unbalanced and excessive nutrition on human development need to
be considered across a broad spectrum.
Key message
Unbalanced nutrition can result from both inadequate and excessive dietary intakes, and both
can exist at the same time in many populations. Moreover diets which lead to over-nutrition
(eg excess calories) are often micronutrient poor.
Nutritional transitions and patterns of chronic disease

Human diets have changed substantially during the course of our evolution and history.
Compared with current diets, the pre-agricultural hunter-gatherer diets of our Palaeolithic
ancestors were based on wild animal and plant foods and were much higher in protein and
lower in carbohydrate (see Figure 1).

Figure 1: The human dietary transition
Hunter-gatherer energy sources USA energy sources
65% Fruits 17%

Fruits 55% Vegetables
Vegetables Legumes
Lean game Nuts Cereal grains
Nuts
Wild fowl Honey Milk,
35%
Eggs milk products Fatty meat
Fish Sugar, sweeteners Poultry Eggs
Shellfish Separated fats Fish
Alcohol Shellfish
28%
A typical hunter-gatherer diet versus a typical modern USA diet.
Estimated dietary components in Palaeolithic human ancestors, based in part on hunter-gatherer diets,
compared with those in contemporary United States of America (USA). Note the relatively high protein and low
carbohydrate content of the hunter-gatherer diet.
Source: Eaton SB & Cordain L (1997) Evolutionary aspects of diet: old genes, new fuels. Nutritional changes
since agriculture. World Review of Nutrition and Dietetics 81: 26-37. Modified after Cordain L, Eaton SB,
Brand Miller J et al (2002) The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic.
European Journal of Clinical Nutrition 56: S42-52.
The introduction of agriculture 10,000 years ago permanently changed the nature of our food
supply, as plants and animals were domesticated for the first time. Further dietary change followed
the Industrial Revolution, which created opportunities to process foods such as grains and cereals;
and the onset of global trading introduced new foods into the UK diet. Our dietary patterns have
continued to evolve to the present day as new food products have become available and we are
influenced by dietary trends occurring in other parts of the world.
Although it is argued that this rate of change in diet from Palaeolithic times has been too fast to
allow the human genome to adapt, and is linked to the rising incidence of chronic diseases,5 many
of the improvements in nutrition in the UK over the last century have had an enormous beneficial
impact on mortality and public health. Diseases such as goitre or rickets, which were historically
associated with social deprivation and malnutrition, are now rarely seen. Improved nutrition has
therefore played a role in the dramatic increase in life expectancy. Some recent trends, however,
are a cause for concern, such as the increase in the sugar and salt content of the diet. These
recent dietary changes have also been accompanied by reductions in physical activity, and there is
considerable concern about the consequences of the combined effects of these changes on the
incidence and patterns of obesity and associated diseases.

What is good nutrition?

Good nutrition implies that the bodys needs for energy and nutrients, from the macronutrients
protein, carbohydrate and fats to the micronutrients such as vitamins and trace elements, are
being met by the diet. The bodys needs for nutrients arise from a wide range of processes. The
most immediately obvious are linked to basal metabolism such as the need for dietary fat and
carbohydrate to produce energy, and thiamine (vitamin B1) in its active pyrophosphate form as a
cofactor in oxidative decarboxylation of pyruvic acid and -ketoglutaric acid. Although physical
activity and work require energy, the greater part of our need for dietary energy is to support basal
metabolism. Nutrient intake needs to be sufficient to maintain body reserves and to replace the
turnover of components such as muscle proteins that are broken down during normal function.
An adequate nutrient intake is essential for immunity; nutritional status and the intake of nutrients
such as n-3 polyunsaturated fatty acids, antioxidant nutrients and zinc affect immune function
and the activities of the immune system may themselves have negative effects on nutritional
status. Finally, nutrient requirements are increased during pregnancy, and during postnatal growth
and development. The many functions of nutrients means that adequate nutrition is central to
metabolic integrity, and of key importance to growth, reproductive function and the maintenance
of good health.
Key message
The many functions of nutrients mean that adequate nutrition is central to metabolic integrity,
and of key importance to growth, reproductive function and the maintenance of good health.
Malnutrition implies that the bodys needs for nutrients are not being met; it also describes an
imbalance of these constituents that can be associated with either inadequate or excessive food
intake. During short periods of insufficient energy supply the body can use reserves, such as fat
and glycogen in liver and muscle, and degrade some tissues to preserve its function. In the longer
term, an insufficient supply of nutrients will become limiting to function. In early life an insufficient
supply of nutrients will result in reduced growth and impaired development. It is noteworthy that
during development these effects may be due to deficiencies in dietary constituents that are not
usually essential in adult life. For example, because the fetal requirements for the non-essential
amino acid glycine are large, it becomes conditionally essential in late gestation and poor nutrition
6
can produce effects of glycine insufficiency.
The developmental consequences of inappropriate nutrition

The focus of this report is on the long-term consequences for health arising from impaired growth
and development in early life both in prenatal life and in early childhood. Every individual has a
blue-print that is genetically determined, and that sets their growth potential; but realisation of
7
this potential is only possible if the nutrient supply during growth is adequate. Among babies
born to chronically malnourished women, low birth weight is relatively common, and stunting in
infancy is prevalent in communities where food supplies are insufficient. Beyond these extreme
examples though, our understanding of the importance of variations in diet and nutritional status,
such as those seen in the UK population, and how these impact on early development, is limited.
Babies continue to be born and to survive in populations that are chronically malnourished, and
nutrient supplementation studies carried out in these communities often result in small changes in
8, 9
birth size. In the past it might have been concluded that prenatal growth is largely protected
from variations in maternal diet and nutritional status. We now know that variations in birth size,
that we describe as being within the normal range, are predictive of disease incidence much later

in life and that this is evident even in developed communities such as the UK. Within this range,
lower birth weight and impaired early growth are linked to an increased occurrence of chronic
10
conditions such as cardiovascular disease and type 2 diabetes in adult life.
The importance of development for later health

The discovery that adult chronic disease is linked to low birth weight and poor weight gain in infancy
11
led Hales and Barker, in 1992, to put forward the thrifty phenotype hypothesis (see Figure 2). The
central element of the hypothesis is that fetal and infant malnutrition are important drivers of the
processes leading to disease in later life. Fetal malnutrition could arise through maternal
malnutrition or failure of the fetal supply line such as placental insufficiency. It was proposed that
malnutrition during these periods of rapid development forced the fetus or infant to become
thrifty and to prioritise limited resources to some tissues at the expense of others. Thus, brain
growth would be supported, but truncal growth, the growth of skeletal muscle, the development
of abdominal organs (liver, pancreas, kidneys) and some parts of the vascular tree would be
deprived. It was also proposed that this altered growth led to permanent changes in the structure
and physiology of many tissues, leading to reduced functional capacity in later life. This reduced
capacity may not be important to individuals who continued to be poorly nourished, but disease
would be triggered more readily by stressors, such as obesity, in later life. Hence if fetal and/or
infant undernutrition resulted in a reduced pancreatic beta cell mass, this would be more likely to
result in type 2 diabetes and the metabolic syndrome if the individual became obese in childhood
or adult life.
Key message
It has been known for many years that unbalanced nutrition during development can cause
long-term consequences leading to permanent changes in the structure and physiology of
many tissues, leading to reduced functional capacity in later life. The consequences of this for
human chronic disease are now increasingly appreciated.

Figure 2: The thrifty phenotype hypothesis
Mothers development and growth impaired
Maternal malnutrition
Maternal hyperglycaemia Other maternal/placental influences
Fetal and infant malnutrition
Changes in growth, metabolism

and vasculature
Hypothalamic
-pituitary
Pancreatic Muscle, liver,
Kidney -adrenal axis and
B-cells adipose tissue
sympathetic
system
Adult B-cell Insulin

Hypertension Renal failure
function resistance
Source: Hales & Barker (2001) The thrifty phenotype hypothesis: type 2 diabetes. British Medical Bulletin 60: 5-20.
It is now thought that the responses to fetal malnutrition not only alter key organs to ensure survival
at that time, but also set in train metabolic adaptations that could improve postnatal survival. The
mother in effect gives the fetus and infant a forecast of the nutrition it can expect after birth, so
that its metabolism can develop to match the environment into which it is born. These adaptations
12
only become detrimental when the postnatal environment differs from that predicted.
13
This is the reasoning behind the mismatch model of increased risk of chronic disease (see Figure 3).
The use of such terms as forecast or predicted in this context does not imply that it is a conscious
process. It involves fundamental processes of developmental plasticity common to many other species.
The cues for such predictions come from the developmental environment and nutritional cues are of
paramount importance. Development comprises critical periods in which plasticity operates over a
defined period of time, and after this critical period for an organ or system has elapsed, the
characteristics of the organism (their phenotype) is fixed (see Box 1). For example, the maturation of the
heart muscle cells in humans is completed before birth; there is limited capacity to increase the number
of cardiomyocytes postnatally and increases in cardiac muscle mass can only be achieved by hypertrophy
of existing cells. This can place them at additional strain and predispose to later heart failure.

Box 1: The impact of phenotypic adaptation on human health
The period of human development is one when the individual attempts to match the structure
and function of their organs and tissues to the world they expect to inhabit, particularly the
future nutritional environment. These processes are unique to development and may be
irreversible. It is for this reason that fetal and infant nutrition is particularly important to future
health. Early interventions are not only more likely to be more efficacious in preventing disease
than later interventions it is possible that later interventions may be ineffective. This is
because some phenotypic attributes which confer risk of later disease are established in
development. Clearly intervention to prevent them can only be made during development
itself. This is why understanding the developmental processes involved and how they may be
optimised during human development is an urgent priority for promoting human health.
According to the mismatch model, the risk of chronic disease will be greatest when there are
extreme transitions from one nutritional environment to another, either within an individuals own
lifetime or between generations. This is borne out by the high risk of disease in migrants from poor
environments in developing countries to the richer environments of the West. It also emphasises
that the risk will be high in populations that start from a low nutritional plane, even if the transition
does not place them at a nutritional level that would be considered rich by Western standards.
Hence the speed of change in developing countries experiencing economic progress is producing
disease in individuals who are younger, and relatively less obese, than in the developed world.
Figure 3: Mismatch model of chronic disease
Nutritional/energy balance
Plentiful
Increasing risk
Adult environment
of disease from
unpredicted excess
Healthy range
Epigenetic processes
attempt to achieve match
Sparse
Optimal Impaired
Developmental environment
Source: Gluckman PD & Hanson MA (2004) Living with the past: evolution, development, and patterns of
disease. Science 305: 1733-6.

Over the course of our evolution, humans have adapted to a range of environments,
including nutritional and physical activity levels. Within this range (grey zone) we should meet
environmental challenges and remain healthy. Outside this range, the risk of disease increases both
from inadequate and excessive nutrient/energy level (red lines). Cues from the developmental
environment before birth and in infancy alter the phenotype of the person, using epigenetic
processes, and hence set their adaptive range. Thus an impaired developmental environment
increases the risk of disease due to a phenotype not being well matched to the environment.
Key message
Ill-health can result when a person cannot respond adequately to the challenges their lifestyle
presents. The settings of these responses are established in part during fetal and infant life,
based on nutrition during these periods.
Obesity
Obesity is one of the most important problems of our time. The incidence is increasing rapidly all
over the world. The rising levels of obesity in the UK, particularly among children, and the
significant impact that this will have on the future health of the population are of concern to
politicians and healthcare professionals alike. The prevalence of obesity is now so high that it is
commonly referred to as an epidemic (see Box 2).
Box 2: Prevalence of overweight and obesity in the UK
In England in 2003, 22 per cent of men and 23 per cent of women were obese and a
14
further 43 per cent of men and 33 per cent of women were overweight.
In England in 2003, more than 2.5 million children aged two to 15 were either overweight
14
or obese.
15
In Scotland in 2003, one in five (22%) of children aged 11-12 were obese.
The 2005/06 Welsh health survey reported 56 per cent of adults were classified as
16
overweight or obese; 61 per cent of men compared with 51 per cent of women.
The Northern Ireland health and social wellbeing survey 2005/06 reported 59 per cent of
adults were classified as overweight or obese; 64 per cent of men compared with 54 per
17
cent of women.
The Scottish health survey 2003 reported 65 per cent of men and 60 per cent women were
15
classified as overweight or obese.
Recent estimates suggest that without action, by 2050, 60 per cent of men, 50 per cent of
women and 25 per cent of all children under-16 could be obese. The financial impact of this
18
to the NHS alone could be an additional 5.5 billion per year at current prices.

Overweight and obesity in developing countries

Economic development and improvements in agricultural production are transforming the
nutritional situation for children and adults in developing countries, although rising food prices
and continued food insecurity are a concern. Undernutrition, wasting, stunting and micronutrient
3
deficiencies are still major problems in developing countries, and occurring in early life, they
19
cause long-term damage to human capital and health. Improved availability of energy-rich
foods has however, enabled large numbers of people to escape from hunger. This has brought
considerable benefits, but is already giving rise to obesity and obesity-related disease. Developing
countries are reporting high rates of coronary heart disease (CHD) and type 2 diabetes that have
appeared in one or two generations to become leading causes of morbidity and mortality. These
20
epidemics are expected to intensify. By the year 2030, the prevalence of diabetes is predicted to
rise by over 100 per cent in India, China, sub-Saharan Africa, Latin America, the Caribbean and
the Middle East; an increase far exceeding that in high-income countries (54%). The highest
number of people with diabetes will be of working age (45-64 years) unlike developed countries,
where the greatest numbers are in older age groups, and in addition diabetes in pregnancy will
become a common problem. There are similar increases anticipated in hypertension, CHD and
21 21
stroke. By 2015, an estimated 20 million people will die from cardiovascular disease every year.
In the context of this report on early life nutrition, obesity is important in a number of ways. Firstly,
as described, obesity arising during childhood or adult life, can unmask the effects of adaptations
induced by undernutrition during fetal life or infancy.
Secondly, there is good evidence that increased adiposity and/or an adverse distribution of body fat
is itself an outcome of malnutrition (both undernutrition and excessive nutrition) in early life.
22
Adults who had a lower birth weight have been shown to have a higher waist circumference.
Low birth weight babies born to underweight women in India are excessively adipose relative to
23
their body weight. In experimental animals, maternal undernutrition during pregnancy is
24
associated with increased adiposity in the adult offspring. The mechanisms for this phenomenon
are unknown, but may arise when the correct balance of nutrients required for tissue synthesis is
25
not available, leading to energy storage as adipose tissue.
Maternal obesity, another form of maternal malnutrition, also increases the adiposity of the fetus
and newborn baby. This phenomenon is exacerbated further if maternal obesity is complicated by
gestational diabetes, an example of fetal overnutrition in which maternal glucose, freely crossing
the placenta, stimulates fetal insulin secretion and adipose tissue deposition. It is known that
maternal gestational diabetes is a risk factor for early-onset type 2 diabetes in the offspring, and
recent data suggest that maternal obesity alone, even in the absence of gestational diabetes,
26
increase the risks of metabolic syndrome in the offspring. A recent follow-up study of more than
9,000 women with normal glucose tolerance at initial screening, found that increasing maternal
glycaemia was associated with a greater risk of obesity in the children, even amongst children of
normal birth weight. Importantly, among those who fulfilled criteria for gestational diabetes, the
relationship between maternal glycaemia and offspring obesity was lost if the mother received
27
treatment. Maternal obesity is an increasing problem worldwide, and it seems likely that this will
contribute increasingly to the burden of diabetes in the future. Gestational diabetes is an example
of how susceptibility to diabetes can be transmitted non-genetically from one generation to the
next. Women who were themselves of low birth weight are at increased risk of developing
28
gestational diabetes, especially if they become obese in adult life.

Nutrition during infancy also determines later risk of obesity. Rates of overweight and obesity are
lower in people who were breastfed, although there is debate as to whether this is a causal
relationship. Rapid weight gain in infancy also predicts an increased risk of obesity.
Key message
The increasing incidence of obesity will have adverse consequences for the development and
health of future generations.
Previous work by the BMA

The BMA recognises the importance of nutrition during early life. Before and during pregnancy it is
vital that women eat healthily in order to maintain their health and for the pregnancy to develop
successfully. A childs diet during infancy can also impact significantly on their health, growth and
development, and on their health in adulthood. Evidence suggests that early life nutrition
influences an individuals risk of adult CHD, diabetes, stroke, asthma and cancer; and has long-
term effects on bone health, muscle function, immune and cognitive function and rates of ageing.
These relationships may result from either under- or overnutrition in early life.
29
The BMA publication Growing up in Britain (1999) reviews the nutritional needs of children from
birth to age five and the health consequences of poor nutrition, including the effects on growth
and cognitive development. It highlights the importance of breastfeeding and raises concerns
about the need to increase breastfeeding rates in the UK including addressing the inequalities in
breastfeeding between socio-economic groupings. This report also discusses the evidence that
influences which act in fetal and infant life permanently set structures and metabolic processes in
29
the body. In particular it highlights evidence of a link between undernutrition in utero, low birth
weight and later risk of CHD. Growing up in Britain makes a number of recommendations about
ways in which inequalities in child health should be tackled. In relation to nutrition it states that:
ensuring good standards of nutrition and advice on healthy eating for young women and their
babies must be a priority for Government action with the provision of a safety net for children at
nutritional risk, for example, by providing free nursery and school milk, fruit and a balanced meal.
Government-led strategy should be developed to improve diets of infants and young children
and help prevent anaemia, dental caries and obesity. Particular efforts should be focused on
increasing breastfeeding rates and improving the quality of weaning diets; breastfeeding should
be actively promoted by Government and health professionals, to employers as well as parents,
and the benefits monitored.
Many of the themes from the 1999 report are revisited here to establish current thinking about the
relationship between early life nutrition and later health; to what degree inequalities in nutrition
still exist; and what factors are influential in determining consumption patterns. Concerns about
the future health of children have grown further since its publication. Public health initiatives are
now focusing attention on the importance of maternal and infant nutrition, both in relation to
poor and unbalanced diet and also to overnutrition. This is true in both developed counties such as
the UK and also in the developing world. Further research, dissemination of the evidence and
discussion of the health promotion policy necessary are urgently needed.

Conclusions
Balanced nutrition during human development is of critical importance for later health and
wellbeing and for reducing the risks of many chronic diseases.
Unbalanced nutrition can result from diets which have either excessive or inadequate
nutrient intakes. Energy dense diets can nonetheless be poor in micronutrients.
The consequences of unbalanced nutrition at both ends of the dietary range are associated
with increased risks of adult chronic disease.
Humans evolved to consume a diet very different from that consumed by many people
today. This makes our physiology potentially mismatched to our contemporary lifestyles,
increasing the risks of ill-health.
During development, humans like other animals attempt to match the structure and
functions of their organs and tissues to the world in which they expect to live. The
prediction is based on cues from the mothers environment via the placenta and her milk.
Inaccurate predictions, for example, through socio-economic change leading to a nutritional

transition between generations, increase mismatch and risk of disease.
In addition to maternal undernutrition, the rising incidence of maternal obesity and diabetes
in pregnancy will exacerbate the epidemic of chronic disease in developed societies.
As low income countries develop, the cycle of diseases such as diabetes and obesity
triggered by nutritional mismatch may be followed by further cycles arising from relative
overnutrition during fetal and infant development.

Chapter 2: Fetal nutrition: impact on

development and later life
Having a nutritious diet during pregnancy helps to protect the mothers health and to control her
level of weight gain. Current UK recommendations for diet before and during pregnancy are given
in Appendix 3. The embryo and fetus receive all their nutrients directly from the mother; good
maternal nutrition is therefore imperative for optimal prenatal development. Unbalanced nutrition
will also cause metabolic and hormonal changes in the mother. In animal models this can affect
the allocation of stem cells, embryonic and placental lineages, and have long-term effects on
offspring growth and health. In humans, maternal diet and body composition affect the growth of
the early embryo making a focus on diet before pregnancy as important as that during pregnancy.
Later in gestation, when fetal growth is maximal, undernutrition leads to a range of adaptive
responses such as redistribution of blood flow in the fetal body and changes in the production of
30
fetal and placental hormones which control growth. These responses may include changes in
31
placental transport function, an area of research about which we currently know relatively little.
Even without changes in overall fetal body size, the growth of certain organs such as the heart and
kidney can be altered. Thus even fetuses of normal birth size may have mounted adaptive
responses to unbalanced nutrition and are therefore phenotypically altered. If the nutritional
challenge is too great or too prolonged for these adaptive responses to cope, eventually slowing in
overall fetal body growth must result, leading to low birth weight. In late gestation this growth
restriction is likely to be asymmetrical, with the head being less affected than the body.
Impact of fetal nutrition on health in later life: the developmental

origins concept
The developmental origins of disease concept has a long history. The seminal studies of Dorner and
32 33
colleagues linked pre- and postnatal nutrition to later risks of obesity, arteriosclerosis and
34, 35
diabetes and Gennser et al showed that blood pressure was higher in men of low birth
36
weight. Forsdahls study of Norwegian populations showed that a poor childhood environment
was associated with increased chronic adult disease, even if the persons circumstances improved in
37
later years. Similarly, Lucas had proposed that detrimental influences in early life may increase risk
38
for later disease. The most well-known reports, however, are those from Barker and his
colleagues in the 1980s, showing an association between low birth weight and risk of later
cardiovascular disease in middle-aged men and women in the UK for whom detailed birth records
39
were available. These early papers from Barker and colleagues were followed by others showing
that low birth weight was not only associated with increased risk of death from cardiovascular
disease but of also hypertension, insulin resistance, type 2 diabetes, dyslipidaemia and central
40
obesity; in fact each of the criteria which define the metabolic syndrome.
Key message
Low birth weight is associated with increased risk of death from cardiovascular disease,
hypertension, insulin resistance, type 2 diabetes, dyslipidaemia and central obesity.

Box 3: Fetal programming
In this context the term fetal programming is widely used. It is somewhat misleading, as it
implies deterministic mechanisms, similar to its original use for the genetic programme for
41
development. It suggests analogy with a computer programme which, once running, cannot
be altered. There is now more use of the terms programming and reprogramming to refer to
42
the processes by which stem cells become pluripotent during embryonic life. This is in line
with the original use, as it suggests switches between predetermined developmental
pathways, enabling embryonic stem cells to differentiate to lung, liver, lymphocytes, etc. The
use of fetal programming or programming of disease is at odds with the plastic nature of
adaptive responses by the embryo, fetus and infant and also underplays the role of later
environment in exacerbating the risk of disease. Developmental origins of disease, or induction
of risk of disease are more accurate terms for this process.
The validity of the concept of the developmental origins of disease has been questioned because
of the wide variability reported among associations between birth weight and proxy markers of
43
disease such as later blood pressure, however associations are much stronger when the outcome
44
measure is clinical disease. Interpretation is also influenced by the recognition that pregnancies in
the historical cohorts occurred when nutrition and healthcare were very different from those of
contemporary developed societies. The lower birth weight individuals in these cohorts, for
example, would be unlikely to include very pre-term or intrauterine growth restriction (IUGR)
fetuses, or the higher birth weight group to include fetuses of diabetic mothers. Another criticism
has concerned the size of the associations between indices of the developmental environment
40
such as birth weight and later markers of disease. A meta-analysis suggests for example that,
even if causal, a large (1kg) increase in birth weight would be associated with only a 10 to 20 per
cent reduction in adult ischaemic heart disease across the population. This assumes, however, that
birth weight is the exposure of interest. The hypotheses relating fetal nutrition and growth to later
disease suggest that birth weight, a crude summary of fetal development, is likely to be a distant
reflection of the cellular and molecular processes affected by intra-uterine environment. For disease
45
such as type 2 diabetes, childhood obesity has a large exacerbating effect.
Correction for adult BMI is another area which has proved controversial. There is an association
between larger size at birth and increased adult BMI (itself a strong risk factor for type 2 diabetes
and cardiovascular disease). Since the associations between size at birth and adult diseases are in
the opposite direction, when adjusting these associations for adult BMI the effect of small size at
birth appears stronger. The interpretation of this effect is controversial; it could indicate that an
adverse effect of small size at birth is revealed more clearly by removing the influence of adult BMI,
or it could indicate that the key insult is the transition from being a small baby to being an obese
46
adult as in the mismatch concept (see Figure 3). It is impossible to distinguish between these two
possibilities using observational data. The evidence actually suggests that both of these scenarios
apply. Many studies have shown adverse effects of small size at birth on adult disease without
47-49
adjustment for BMI (see Figure 4).

Figure 4: Patterns of infant and childhood growth associated with later heart disease
Body mass index 0.05

Weight
Height
COHORT
0
Standard deviation (z score)
-0.05
-0.1
-0.15
-0.2
-0.25
0 1 2 3 4 5 6 7 8 9 10 11 12
Age (years)
Growth (shown as Z score, ie shift in standard deviation from the group mean shown as 0) in 357 boys who
developed CHD from a cohort of 4,630 born in Helsinki between 1934 and 1944. Their childhood growth
pattern is characterised by small size at birth, slow growth in years 0-2, then relatively greater increase in
weight and BMI.
Source: Eriksson JG, Forsn T, Tuomilehto J et al (2001) Early growth and coronary heart disease in later life:
longitudinal study. British Medical Journal 322: 949-53
There is also clear evidence of adverse effects of excessive weight gain in childhood on adult disease
risk (see Figure 5) but controversy about the effect of weight gain during infancy (see Chapter 3).
Given the similarities in responses between humans and other animals in terms of adaptive
responses to environmental challenges during development, it may be helpful to consider them in
terms of the spectrum of effects which might be produced on theoretical grounds (see Figure 5).
This is important because it shows how even a modest nutritional challenge during development
might be expected to have long-term consequences, even without an effect on birth weight.

Figure 5: Graded effects of nutrition in development on later function
Developmental Reduced Predictive adaptive responses Damage

disruption reproductive due to
success excess
(coping
/trade-offs)
Good
Later survival,
`
health and
reproductive fitness
Poor
very low very high
Nutritional plane
Link between the nutritional plane in development and effect on later health and fitness. Different types of
effect are produced, depending on the severity of the challenge (and also its timing and duration, not
shown). They can be grouped into:
those where an environmental challenge is so great that it causes a disruption of development, akin to a
teratogenic effect. This is rare for unbalanced nutrition
a less severe challenge but one which nonetheless reduces overall fetal growth and hence birth weight.
The offspring has to cope with the detrimental effects of this in later life
responses to a less severe challenge, which alter the phenotype of the offspring in prediction of its later
environment. Such responses are in the majority across the range of human development, and produce
risk of disease when the induced phenotype is not matched to the adult environment
50
responses to overnutrition in development; this category is becoming increasingly common.
Source: Gluckman PD, Hanson MA, Spencer HG et al (2005) Environmental influences during development and
their later consequences for health and disease: implications for the interpretation of empirical studies.
Proceedings of the Royal Society 272: 671-7.
Many studies, including those from countries other than the UK, have replicated the original association
51
between lower birth weight and death from ischaemic heart disease and also with non-fatal coronary
52
artery disease and stroke. A recent study of 13,830 men and women from the Finnish National Death
53
Register showed an association between low birth weight and all cause mortality among women. A
study of 10,803 children born in Aberdeen in the 1950s has confirmed an inverse association between

54
birth weight and later coronary artery disease and stroke. This is important because the 1950s was a
time when environmental influences were relatively favourable for infants compared with earlier studies,
and so the results may have contemporary relevance. Large cohort studies, such as that of almost
90,000 Swedish army recruits born between 1973 and 1981, also show that lower birth weight is
linked to higher adulthood blood pressure and, although small in magnitude, the difference was
55
independent of socio-economic factors or familial effects. Even a small rise in blood pressure is
56
important when viewed from the perspective of risk of later disease. A recent meta-analysis of data
from 198,000 individuals from 20 Nordic studies (cohorts of people born between 1910 and 1987)
shows unequivocally an inverse and linear association between birth weight in males, but a U shaped
relationship with females; those of a birth weight higher than 4kg having a higher systolic blood
57
pressure (SBP) in adult life. Similar confirmation of the association with low birth weight and raised SBP
58
has been derived from a British birth cohort study of 3,157 men and women born in 1946.
A recent review of the literature investigating associations between low birth weight and insulin
resistance shows that people who were light at birth generally have an adverse profile of later
glucose and insulin metabolism, which is related to insulin resistance rather than altered insulin
59
secretion. This may be related to the development of body composition; low birth weight in the
Hertfordshire cohort was associated with reduced skeletal muscle mass and increased abdominal
60
fat in adult men.
Mechanisms by which fetal nutrition affects risk of later disease

The concept of developmental origins of health and disease has stimulated wide ranging
investigations into the underlying mechanisms. These investigations have now revealed a great deal
of information on the processes involved, and their operation during critical periods of development
during fetal and infant life. The fetus is at the end of a long supply line for nutrient delivery from its
mother (see Figure 6) so there are several points at which its nutrition might be impaired.
Figure 6: The fetal supply line for nutrients
Mothers diet
Her body composition
Metabolism
Hormonal status
Nutrients in maternal
bloodstream
Placental
Placental metabolism
barrier/transport
Nutrients in fetal
bloodstream
Many processes intervene between the Delivery to developing

food consumed by the mother and the organs and tissues
delivery of nutrients to the fetal tissues.

61-63
Most of the mechanisms have been investigated using animal models. Studies in rats, mice,
sheep, guinea pigs and in non-human primates all lend strong support to the developmental
origins of health and disease hypothesis. Most notably, several characteristics of the offspring
phenotypes arising from a range of maternal nutritional interventions, both by undernutrition and
overnutrition, are shared across species. It has proved remarkably easy to demonstrate
characteristics equivalent to human disease, particularly features of the metabolic syndrome,
through experimental manipulation of the diet of the pregnant animal or her offspring. The effects
include cardiovascular and renal dysfunction, insulin resistance, glucose intolerance, hyperphagia,
64
altered stress responses and even preference for food high in fat and sugar in the offspring.
65, 66
Adulthood adiposity has also been induced. The behavioural effects on the offspring include
67
reduced exploratory behaviour, activity levels and even impaired learning behaviour. These animal
models offer the potential for investigation of mechanisms, leading to suggestions for intervention.
To date the most effective interventions reported have been supplementation of a low protein diet
68, 69 70
during pregnancy in the rat with glycine or folate or treatment of the pups neonatally with
71
leptin. The adverse effects on the offspring of feeding a high fat diet in pregnancy can be
72
reduced by giving a statin to the pregnant animal in late gestation. Animal investigations reveal
that the transmission of risk factors can be passed to more than just the next generation. After a
nutritional challenge to animals during pregnancy effects were seen in their grand-offspring, even
73-75
without a further nutritional challenge.
Key message
Unbalanced nutrition during development can lead to greater risks of chronic disease in
successive generations.
One of the most striking perceptions to arise from recent experimental work in this area is that the
effects of relatively modest dietary restriction or imbalance can affect offspring development and
have long-term consequences for health even when they are administered to the pregnant animal
in either the periconceptional period, or in early pregnancy. At this time they do not invariably
76
affect fetal growth or birth weight. They operate via effects on embryonic stem cell allocation
77
or yolk sac function, and have long-term effects on cardiovascular, endocrine and metabolic
78-82 83
function. Embryo transfer experiments also reveal long-term effects on these systems
and this raises questions about the long-term consequences of assisted reproductive technologies.
These observations are of general relevance because a high proportion of pregnancies are unplanned,
and thus dietary and other effects can be exerted well before the woman realises that she is pregnant.
Epigenetic mechanisms
The environmental effects on the embryo referred to above suggest in particular that epigenetic
processes may be involved. The processes of phenotypic induction through developmental plasticity
produce integrated changes in a range of organs via epigenetic processes. The term epigenetic
84
was coined by Waddington in about 1942 to refer to the ways in which the developmental
85
environment can influence the mature phenotype. His work and that of others on developmental
plasticity stemmed from observations that environmental influences during development could
induce alternative phenotypes from a genotype. They establish a life-course strategy for meeting
12
the demands of the predicted later environment. This explains why impaired early nutrition
produces a range of effects. These include alterations in cardiovascular and metabolic homeostasis,
growth and body composition, cognitive and behavioural development, reproductive function,
repair processes and longevity some of which are associated with increased risk of chronic

diseases including cardiovascular and metabolic disease, precocious puberty, osteoporosis

and some forms of cancer. Understanding the epigenetic processes thus holds the key to
understanding the underlying pathophysiology and to developing approaches to early diagnosis,
prevention and treatment of these diseases (see Appendix 1).
Maternal undernutrition and long-term outcomes in the offspring

Newborn size is related to maternal energy balance, increasing with the mothers BMI and
adiposity. Her height, and independently leg length, head circumference and birth weight, predict
the babys size, suggesting that her own early nutritional biology influences how she nourishes the
86, 87
fetus. The fetal origins hypothesis proposed that maternal ill health, poverty and undernutrition
88
impair fetal and infant growth and were root causes of adult chronic disease. If this is so, indices
of poor maternal nutrition would be associated with cardiovascular disease or its risk factors in the
offspring. So far, unfortunately, there are only crude data available to test this.
There is very little evidence concerning the effects of maternal undernutrition and nutrition in the
developing world on the longer term health of the offspring. Studies in developing or historically
poor countries have shown that low maternal weight, BMI or skinfold thickness in pregnancy are
89, 90 91, 92 93
associated with higher offspring blood pressure, insulin resistance and risk of CHD. Follow-
up of people exposed to the 1944-45 Dutch Hunger Winter showed that exposure of the mother
to acute famine was associated with increased cardiovascular risk in the adult offspring. Outcomes
94
varied according to the timing of famine exposure; late gestation exposure was associated with
greater risk of glucose intolerance and early gestation exposure with obesity, atherogenic lipid
profiles and CHD. Famine effects were independent of birth weight, suggesting that maternal
undernutrition may impair adult health without reducing size at birth.
The Institute of Nutrition of Central America and Panama (INCAP) trial in Guatemala (1969-77) is
the only randomised trial of a nutritional intervention in which cardiovascular risk factors have been
95
measured in the adult offspring. In the original trial, pregnant women and children received one of
two supplements: a high-protein, high-energy drink or a lower nutrient drink. There was no
difference in birth weight between these two groups but the children of mothers who received a
high-protein, high-energy drink had lower blood triglyceride and higher high-density lipid (HDL)
cholesterol concentrations in adult life (profiles usually associated with better cardiovascular health).
The Pune Maternal Nutrition Study was set up specifically to investigate the relationship of
maternal nutrition to the childrens future risk of diabetes and heart disease. It collected
prospective information on diet, workload and micronutrient status in pregnant women in rural
Indian villages. At six years of age the children were thin by international standards but had a
higher percentage body fat than European children. Maternal folate concentrations predicted
higher insulin resistance in the child, and children born to mothers with the lowest vitamin B12
96, 97
concentrations and highest folate concentrations were the most insulin resistant. Thus an
imbalance in the mother in two vitamins important in methyl group provision predicted higher
adiposity and insulin resistance in the child, suggesting an important role for 1-carbon metabolism
in the developmental origins of type 2 diabetes.

Associations between maternal obesity, diabetes, raised birth weight and

adulthood disease
98
The rising birth weight in developed countries (with the possible exception of Japan) associated with
the increasing incidence of obesity in pregnancy and related gestational diabetes, also has potential for
99, 100
detrimental influences on the developing child. There is a U shaped relationship between birth weight
59, 101
and later insulin resistance and obesity, and there is now good evidence that children of women who
are diabetic in pregnancy are themselves more likely to develop insulin resistance in later life and to
96
become overweight. Initially shown in the Pima Indians, a population with a very high incidence of
102
diabetes, this seems to occur in all populations. School children in Taiwan showed a similar phenomenon
103
and Indian children of gestationally diabetic mothers had increased adiposity and hyperinsulinaemia.
While this may represent in part a genetically inherited disorder, studies of sibling pairs discordant for
maternal diabetes show that the effect occurs only in the offspring prenatally exposed to diabetes, strongly
104, 105
suggesting a diabetic trait acquired during development. Infants of mothers with gestational diabetes
106
have a greater neonatal fat mass independent of birth weight and it is reported that a high rate of
childhood metabolic syndrome (central adiposity, insulin resistance and hypertension) occurs in large-for-
26
gestational-age (LGA) babies born to mothers with gestational diabetes compared with appropriate-for-
gestational-age (AGA) babies. Importantly, the risk of metabolic syndrome is also present, but to a lesser
extent, in LGA babies from normoglycaemic mothers. In a recent trial of two diets, normoglycaemic
107
mothers on a high glycaemic index diet gave birth to more LGA babies. Children of mothers with higher
27
glucose concentrations within the normal range are more adipose. Higher birth weight in
normoglycaemic pregnancies is generally associated with raised adulthood BMI, and larger babies tend to
become heavier adults. Although detailed investigations of the relative contributions of lean and fat mass
108, 109
have sometimes suggested that this association reflects increased lean body mass rather that fat mass,
a recent study of infants from obese normoglycaemic mothers shows clear evidence of increased
110
adiposity. To date there have been few attempts to define accurately the relationship between maternal,
childhood and adulthood body composition over any range of maternal BMI. Ongoing prospective
longitudinal studies in contemporary cohorts such as the Avon Longitudinal Study of Parents and Children
111 112
(ALSPAC) cohort in Avon UK and the Southampton Womens Survey (SWS) will be very informative in
this regard. In the latter it is already clear that mothers body composition and dietary balance before
113
pregnancy can affect fetal cardiovascular development in late gestation.
Key message
Extremes of maternal body composition, either excessive thinness or obesity, are associated with
adverse patterns of fetal and infant development leading to poorer long-term health.
Transgenerational effects
There is concern that the detrimental effects of the nutritional transition in many populations
around the world will have an effect on the risk of chronic disease which will persist for several
generations. Animal studies show that a dietary or glucocorticoid challenge administered in
pregnancy can have effects on the metabolism, cardiovascular function and gene expression in the
74, 114
grand-offspring, even without any additional challenge in the second generation. The effects
73
can involve epigenetic changes. Similar changes have been reported in humans exposed to poor
115
nutrition during childhood development including the intriguing possibility that the effects can
be transmitted through the paternal as well as the maternal line. There is now much interest in the
concept that non-genomic inheritance can affect more than one successive generation, both from
75
scientific, social and medical perspectives.

Taking a multigenerational perspective also focuses attention on the ways in which disease risk
can be transmitted during periods of nutritional transition (see Figure 7). Obesity, type 2 diabetes
and altered metabolism in women resulting from poor nutrition during development can result in
greater glucose levels or gestational diabetes in pregnancy. This is likely to induce similar metabolic
changes in their offspring.
Figure 7: Cycles of disease risk
Intergenerational switching of pathways
Gestational
Large babies
diabetes
Women
malnourished Suboptimal fetal
Low pregnancy development
weight gain
Enriched postnatal
Very poor postnatal
enviroment due to
environment
nutritional transition
Obesity
Insulin
Stunting
resistance
Premature
Material
death and
morbidity
morbidity
Cycles of disease risk can involve more than one generation. Women who are malnourished or who have
sub-optimal body composition and weight gain in pregnancy are more likely to have offspring with stunting and
premature death and morbidity (left part of diagram). This becomes a self-perpetuating cycle. Their offspring are at
higher risk of cardiovascular and metabolic disease, especially if socio-economic transition or migration gives access
to high fat and glycaemic index food and reduced physical activity. Women of this generation are more likely to
develop gestational diabetes and to have offspring which in turn are also at risk of obesity and diabetes. This
process, which may involve different mechanisms from the first, nonetheless produces another cycle of disease.
Source: Gluckman PD & Hanson MA (2005) Metabolic disease: evolutionary, developmental and transgenerational
influences. In: Hornstra G, Uauy R, Yang X (eds) The Impact of maternal nutrition on the offspring. Nestle Nutrition
workshop series: Pediatric program. Switzerland: Karger.

Conclusions
Studies of human populations show clear links between early life environment and later
health and disease.
While our knowledge of the specific components of maternal nutrition which produce such
effects is limited in humans, experimental animal studies provide strong evidence that
changing nutrition in the periconceptional period or in pregnancy can produce effects on
the offspring which mimic human chronic disease.
In developed societies, we know that many women consume poor quality diets, which results
on the one hand in nutritional deficiencies and on the other in overweight and obesity.
In developing societies, while maternal undernutrition remains a major problem, maternal

overweight is also of concern.
Development of future interventions will require the identification of biomarkers of poor

developmental nutrition in infants and children.
There is a need for better understanding of the implications of current variations in diet and
nutrition for fetal development and long-term health.
Positive steps need to be taken to ensure that young people understand the importance of
health and wellbeing before pregnancy giving attention to their diet, optimal body
weight, to stopping smoking and to limiting alcohol consumption.

Chapter 3: Infant nutrition
Introduction
Infancy refers to the first one to two years after birth. It is a period of rapid growth in weight,
length and brain size and rapid social, cognitive and motor development. These changes carry high
nutritional needs at a time of total dependence on carers who may have little knowledge about
nutrition or the special requirements of infancy. During the first 12 months of life, the infant must
make a transition from a milk-only diet to one containing the diversity of foods eaten by the rest
of the family. Good nutrition is essential for the infant to maintain and develop its immature
immune defences as it meets pathogens for the first time. Patterns of weight gain and growth,
and nutritional experience, in infancy can have long-term effects on health (see page 40).
Key Message
Infancy is a period of high nutrient requirements, to support rapid growth (including brain
growth) and critical social, cognitive and motor development.
Breast milk is the ideal food for newborn babies and currently in the UK, exclusive breastfeeding is
recommended until the age of six months. Other (often termed complementary) foods are then
introduced and gradually increased in variety and quantity. It is not known what constitutes the
116
ideal diet during this transition but there are well-established guidelines on nutrient requirements
117, 118
and on foods and feeding practice. In the UK, there are wide variations in infant feeding
practices and in how closely parents follow these guidelines (see page 31). For discussion on the
contraindications to breastfeeding see page 35.
In all populations infancy is a period of relatively high mortality. The infant mortality rate (IMR) in
England and Wales (five per 1,000 live births in 2006) has fallen continuously for the past 100
119
years (14.3 in 1976; 105 in 1910). Just over half the deaths are neonatal and related to
120
congenital abnormalities, low birth weight and pre-term birth. There are marked regional
differences in IMR. In 2006, it was highest, 6.4, in the West Midlands and lowest, 4.0, in South
121
West England. There are also strong social class differentials. It is not known to what extent
these inequalities have a nutritional basis.
Developing country perspective on infant nutrition

Infant undernutrition is a huge problem in developing countries. It is estimated that 178 million
(32%) children under five years are stunted, 55 million are wasted, and micronutrient
3
deficiencies are widespread and frequently multiple. Undernutrition causes three million
deaths among children under the age of five in developing countries every year. Infancy is the
period when growth commonly starts to falter and it is difficult to reverse stunting after the
122
age of two years. The main causes are inadequate food (energy, animal protein and
micronutrients) and high rates of infection. Sub-optimal breastfeeding and poor quality
123
complementary foods are key factors. Efforts to improve nutrition in developing countries
should focus on pregnant women and infants to get the maximum benefits for growth,
124, 125
development, health and later economic productivity.

The case for breastfeeding

All current guidelines, including those from the Department of Health (DH), recommend exclusive
breastfeeding for newborns and for the first six months of infancy. Breast milk provides all the
nutrients required at this age in a form that is hygienic and easy to digest. The protein,
carbohydrate and fat profiles are unique to breast milk and differ in many ways from other animal
126
milks. Breast milk also contains a range of bioactive components, including anti-microbial and
126, 127
anti-inflammatory factors, digestive enzymes, hormones and growth factors. Anti-microbial
agents include leucocytes, secretory immunoglobulin (Ig)A, IgM and IgG antibodies, oligosaccharides,
lysozyme, lactoferrin, lipids, fatty acids and mucins. Growth factors are thought to be important
for gut maturation. Lactoferrin is one of several specific binders in human milk that greatly increase
the bioavailability of micronutrients.
Key message
All current guidelines, including those from DH, recommend exclusive breastfeeding for the
first six months after birth.
The volume and composition of breast milk vary with the stage of lactation, within each individual
126
feed, and with maternal nutritional status. Recent research in animals has shown that reduced
128
fetal growth caused by placental insufficiency can impair the quality and quantity of breast milk.
Colostrum, produced during the first few days is low in volume and nutrient content but high in
anti-microbial factors. Volume and nutrient content reach a peak, in mature breast milk, several
weeks after birth. The mothers macronutrient intakes do not have much influence on milk
composition, but her diet does affect the long-chain fatty acid and vitamin content of her milk.
Breastfed infants have more control over the flow of milk than bottle-fed infants. Breastfeeding is
therefore often described as an ideal supply and demand regulation system. The feeding
behaviour of the baby and the quality of the breast milk change with time in a way that may
prevent overfeeding, teach the infant how to recognise satiety signals, and regulate energy intake
differently from formula-fed infants.
The role of leptin in breast milk may be of particular importance in the early development of both
adipose tissue and appetite regulatory systems in the infant, and ultimately on propensity to
obesity in later life. A recent study showed that administration of physiological levels of leptin to
129
suckling rats caused a significantly lower body weight in adulthood. Observational studies have
130
shown that breastfeeding is associated with lower rates of childhood obesity. Bearing in mind
the absence of leptin in formula milk, this may have important implications for the prevention of
obesity in children and in adults.

Current infant feeding practices

The national Infant feeding survey (IFS) is conducted every five years; the latest data are from
131
2005 (see Box 4). These reports provide a wealth of information about variations in feeding
practice, factors that influence the type of milk and duration of milk feeding. They also detail
trends in feeding over time. Exclusive breastfeeding is recommended up to the age of six months
in the UK. The IFS shows, however, that less than 1 per cent of mothers are exclusively
breastfeeding at six months. Current guidelines are to introduce solid foods from six months, to
provide a varied diet that includes starchy foods, fruit and vegetables and meat and fish, and to
encourage the use of home-prepared rather than commercial baby foods (see Appendix 4).
Box 4: The UK Infant feeding survey 2005 findings on breastfeeding
Initial breastfeeding rates in 2005 had increased since 2000 (78% in England, 70% in
Scotland, 67% in Wales, and 63% in Northern Ireland).
Only 48 per cent of mothers were breastfeeding at six weeks and 25 per cent at six months.
45 per cent were breastfeeding exclusively at one week, 21 per cent at six weeks,
7 per cent at four months and <1 per cent at six months.
Three-quarters of mothers had given their baby milk other than breast milk by six weeks,
and 92 per cent by six months.
Just under half of all mothers who had prepared powdered infant formula in the last
seven days had not followed the instructions properly, for example by not using cooled
131
boiled water.
Breastfeeding rates in the UK are much lower than in many European countries for example,
more than 90 per cent of babies in a nationally representative sample studied in Norway were
132
breastfed from birth, and high rates were still present at one, four and six months.
The IFS shows that there are strong relationships between the mothers socio-economic status and
educational attainment and breastfeeding prevalence these factors are associated with both
initiation rates and breastfeeding duration (see Figure 8). In the UK Gateshead Millennium Baby
Study (1999-2000) 84 per cent of mothers with higher education initiated breastfeeding compared
133
with 25 per cent of mothers with no educational qualifications. Percentages still breastfeeding at
four months were 49 per cent and seven per cent. There were also strong negative associations
with Townsend score, a measure of deprivation based on residential postcode.
Key message
Breastfeeding rates in the UK are much lower than in many European countries. Less than
1 per cent of mothers in the UK are exclusively breastfeeding at six months.

Box 5: Reasons why mothers do not breastfeed or cease breastfeeding early

134
A recent focus group study in the UK suggested further detail of the reasons women may
not breastfeed or why they stop breastfeeding early. These were as follows.
The attitude of other people women felt that breastfeeding in public was unacceptable
and embarrassing, while bottle-feeding was accepted by everybody and in all places. A lack
of places to breastfeed out of sight restricted womens ability to get out of the house.
This may be a bigger issue for low-income women, who may not have the option of
breastfeeding in the car. Some women reported breastfeeding in public toilets as the only
option. Women wished that cafs and shops could provide places to breastfeed with some
privacy.
Attitudes of family and friends some women said that even family and friends found
it repulsive to be in the same room when they were breastfeeding. Some grandparents
thought it excluded them from having the chance to feed the new baby. It was clear that
the opinion of family and friends was a stronger influence than that of health practitioners.
Lack of knowledge women vaguely knew that breastfeeding was supposed to be
beneficial, but they could not name any benefits, and were not convinced about them.
In the study only one woman had learnt at school about benefits of breastfeeding; most
did not hear about it until they were pregnant. Feeding was not well covered in antenatal
classes.
Lack of professional support women experienced difficulty in trying to establish
breastfeeding but were unwilling to bother the midwife. Bottle feeding seemed easier.
Experience breastfeeding seemed difficult and painful, and many women experienced
problems ranging from getting the baby latched on, sore nipples, and disturbed sleep.
Women, especially adolescents, complained of a lack of freedom to travel/socialise/work.
Worry about babys weight gain women said that health visitors were always worried
about weight gain.
Although some women in this study mentioned the benefits of breastfeeding including
feelings of wellbeing and relaxation during feeds, convenience (less washing up), and less
expense, it is clear that there are significant barriers for women in the UK which impact on
their choice to breastfeed.
Source: McFadden A & Toole G (2006) Exploring womens views of breastfeeding: a focus group study
within an area with high levels of socio-economic deprivation. Maternal & Child Nutrition 2: 156-68.

Box 6: Reasons given by mothers for stopping breastfeeding by duration of breastfeeding
Babys age when breastfeeding ceased
Less than 1 week, 2 weeks, 6 weeks, 4 months, 6 months, All mothers

1 week less than less than less than less than less than giving up
2 weeks 6 weeks 4 months 6 months 9 months
Percentage (%) of mothers who stopped breastfeeding

Why stopped breastfeeding
Insufficient milk 26 41 53 48 37 24 39
Baby rejected breast 34 21 17 13 11 16 20
Painful breasts/nipples 24 29 17 9 1 2 14
Took too long/tiring 11 17 19 19 5 5 14
Mother was ill 8 11 9 8 5 5 8
Domestic reasons 4 7 9 10 3 2 7
Returned to work/college 1 1 8 15 22 7
Too stressful 7 7 6 4 3 1 5
Baby ill 6 7 5 3 2 1 4
Baby could not be fed by others 1 5 4 6 4 3 4
Did not like breastfeeding 2 5 4 1 1 * 3
Breastfed for as long as intended 1 1 1 4 10 6 3
More settled on formula 1 2 2 4 8 3 3
Baby not gaining weight * 1 2 6 4 3 3
Teething/biting 3 14 2
All Stage 3 mothers who stopped
breastfeeding during survey period 1143 351 1087 1284 195 727 4827
Includes some cases where mothers breastfeeding duration not known

Code introduced at later Stages
* Percentage less than 0.5%
Percentages do not add to 100% as some mothers gave more than one answer
Source: Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The Information Centre.

Figure 8: Prevalence of breastfeeding according to mothers socio-economic classification:

Infant Feeding Survey 2005
100
Managerial &
professional
Intermediate
80
% of mothers breastfeeding
Routine &
manual
60
40
20
0
Birth 2 4 6 8 10
Months
Developing country perspective on breastfeeding

3
As in the UK, breastfeeding rates are sub-optimal in most developing countries. Although more
than 95 per cent of babies overall receive some breastfeeding, rates of exclusive breastfeeding
are only 50 per cent on average up to the age of two months, and 20 to 30 per cent from two
3
to five months.
Complementary feeding practices in the UK

In comparison with milk feeding in UK infants, current variations in complementary feeding practice
and the weaning diet are less well documented. Some information on weaning practice is collected
in the IFS (see Box 7).

Box 7: The UK Infant feeding survey 2005 findings on complementary feeding
In 2005, mothers were introducing solid foods later than in the 2000 survey (51% by four
months compared with 85% by four months respectively).
Very few women (2%) followed DH guidance to delay weaning onto solid foods until six
months.
Babies given solid foods between four and six months were much more likely to be fed
commercially-prepared foods (85%) than home-prepared foods (51%).
Most mothers (92%) avoided the use of salt completely in the diets of their babies.
The proportion of mothers avoiding the use of salt increased between 2000 and 2005 (33%
to 51%), rises were also seen in the proportion avoiding nuts (30% to 48%) and honey
131
(6% to 13%); a greater awareness of food allergies was a key reason for this change.
The IFS showed that in 2005, although there was a decline in prevalence of very early introduction of
solid foods since 2000, most infants had been introduced to solid foods before the recommended
131
age of six months. The main reasons given for the introduction of solid foods before three months
were that the baby was not satisfied with milk alone, or the mothers experience with a previous
baby. Early introduction of solid foods was more common in younger mothers, and among mothers
of lower socio-economic status and lower educational attainment (see Figure 9).
Figure 9: Age by which solids had been introduced according to mothers socio-economic
classification: Infant Feeding Survey 2005
100
Managerial &
professional
Intermediate
80
Routine &
manual
60
%
40
20
0
Birth 1 2 3 4 5 6 7
Months

Among working mothers, delaying return to work until at least six months was associated with
131
later introduction of solid foods.
The nature of the weaning diet varied by mothers socio-economic status. When compared with
other women, mothers in managerial/professional occupations were more likely to feed their
infants cooked vegetables and fruit, rice and pasta, and meat and fish, and less likely to provide
131
regular servings of sweets, biscuits and savoury snacks.
There are two large cohort studies of UK infants in which variations in complementary feeding and
weaning practice and dietary intakes have been assessed: ALSPAC and the Southampton Womens
Survey (SWS). The ALSPAC study collected dietary data using three-day diet diaries for over 1,000
135, 136
infants born in 1991-92. At eight months, 34 per cent of the infants had not eaten any fruit
and 25 per cent had not eaten vegetables in the three-day study period, while 26 per cent of the
infants had eaten chocolate. At 18 months, 16 per cent of the children had not eaten fruit and 8
per cent had not eaten vegetables in the three-day period but 63 per cent of the children had
eaten chocolate and 66 per cent had eaten savoury snacks. Although intakes of most nutrients
were above the reference nutrient intakes (considered adequate for 97% of children), vitamin D
intakes were low at both ages, and iron intakes were low at 18 months.
The ALSPAC study also showed that at 18 months, the most common container for drinks was a
trainer cup. Eighty-six per cent of children had at least one drink from a trainer cup over a 24-hour
period, 64 per cent of children were given at least one drink in a bottle, and 10 per cent solely
used a bottle. Use of a bottle was more common among children who had not been breastfed,
137
who had older siblings, and who had mothers who smoked. Children being fed milk in a bottle
consumed greater volumes when compared with children given milk in a cup; this was particularly
marked for the children only fed by bottle. A wide variety of drinks were given at this age,
including low calorie squashes (48%), tea and coffee (17%), and fizzy drinks (7%). Maternal
education was the most important factor associated with the types of drinks consumed at this age
more highly educated mothers gave their children fruit juices more often, whereas women with
low levels of educational attainment were more likely to give their children tea, coffee and soft
drinks. Seventeen per cent of children whose mothers had Certificate of Secondary Education
(CSE) qualifications or less were given fizzy drinks over a 24-hour period.
More recently the dietary patterns of 1,434 infants born to women in the SWS between 1999-2003
138
were reported. The most important pattern of diet identified at both six months and 12 months
of age was consistent with current infant feeding guidance, and was characterised by high
consumption of vegetables, fruit, meat and fish, and other home-prepared foods. This dietary
pattern was labelled the infant guidelines pattern. Infants who had high scores for this pattern
of feeding were also more likely to have been breastfed. A number of factors, including a range
of maternal and family characteristics were considered as influences on the infants pattern scores.
At both ages the key determinant of the nature of the infant diet was the quality of the mothers
diet. Infants whose mothers had high prudent diet scores and healthier dietary patterns,
139
characterised by high intakes of fruits and vegetables, and wholemeal bread, were more likely to
have a comparable diet, and were fed in accordance with infant feeding guidelines. Conversely,
mothers who had low prudent diet scores and whose diets were characterised by high intakes of
white bread and chips, added sugar and full-fat dairy products, were less likely to provide a diet for
their infant that conformed with infant feeding guidance (see Figure 10). The influence of
mothers dietary pattern on her infants diet was independent of a range of other factors, including
her educational attainment and smoking status.

Key message
In comparison with milk feeding, less attention has been given to the introduction of
nutritious weaning foods. It is known that the quality of the weaning diet for UK infants is
strongly influenced by the socio-economic status and educational attainment of the mother.
Figure 10: 12-month infant guidelines pattern score according to prudent diet score of
the mother
1 P<0.001
12 month infant guidelines score
0.5
-0.5
-1
to -1 to -0.5 to 0 to 0.5 to 1 >
1
Mothers prudent diet score
Source: Robinson S, Marriott L, Poole J et al (2007) Dietary patterns in infancy: the importance of maternal and
family influences on feeding practice. British Journal of Nutrition 98: 1029-37.
Childrens diets and food preferences have been shown to be influenced by their food
140-142
environment, and by the eating behaviours of their parents. The SWS provided evidence that
influences of the food environment on childrens diet operate very early as soon as infants start
to eat solid food. The findings also suggest that interventions to change mothers diets will have
direct consequences for the diets of their children.
Key message
Influences of the food environment including maternal diet operate very early on childrens
diets, from weaning onwards. Interventions to change mothers diets will have direct
consequences for the diets of their children.

Developing country perspective on complementary feeding

Poor-quality complementary feeds are the norm for infants in disadvantaged families and a
major cause of infant stunting. Programmes to support breastfeeding, promote better
complementary feeding and supply micronutrient supplements, are some of the most effective
123
measures that could be taken to reduce undernutrition in these countries.
Guidelines on infant feeding
Breastfeeding guidelines
In 2003, the World Health Organisation (WHO) recommended that all babies should be exclusively
breastfed for the first six months of life (the previous recommendation was four to six months).
Thereafter complementary feeding should be introduced, with breastfeeding continuing as long as
possible up to two years. The evidence underlying the advice to extend exclusive breastfeeding
from four to six months is persuasive in developing countries, but less so for high-income
143-145
countries. Breastfed babies, even in high-income countries, experience significantly fewer
146
episodes of gastro-intestinal and respiratory infection. Benefits to the mother of breastfeeding
include convenience, less expense, a faster return to pre-pregnant weight, delayed onset of
147
ovulation, and possibly long-term protection against breast and ovarian cancer.
Key message
Breastfed babies, even in high-income countries, experience significantly fewer episodes of

gastro-intestinal and respiratory infection compared with formula-fed babies.
The National Service Framework for Children, Young People and Maternity Services highlights the
importance of breastfeeding, and recognises that it is a skill that needs to be taught and
supported. The DH produces a booklet for health professionals on how best to do this entitled
148
Good practice and innovation in breastfeeding.
149
More recently NICE have produced guidance on improving the nutrition of pregnant and
lactating mothers from lower socio-economic groups as a way of targeting those most in need of
advice and support.
Maternal diet during lactation guidelines

For most women in the UK, a normal healthy diet is adequate to support breastfeeding. The Food
150
Standards Agency (FSA) provides specific dietary advice for lactating mothers. Vitamin D
supplements (10 micrograms daily) are recommended. Mothers are advised that fish is good for
their own health and for the development of the baby, but to limit the intake of oily fish to two
portions per week because of mercury levels. If there is a family history of peanut allergy, women
150
are advised to avoid eating peanuts during lactation.

Developing country perspective on maternal diet during lactation

Maternal micronutrient deficiency during lactation (especially for the B vitamins, vitamin A and
151
iodine) can lead to low levels in breast milk. Even undernourished mothers in developing
countries can, however, usually breastfeed successfully, and milk quality appears to be largely
126
unimpaired.
Box 8: Contraindications for breastfeeding
There are some circumstances in which breast milk can contain harmful agents, such as HIV,
environmental pollutants (eg dichlorodiphenyl trichloroethane (DDT), polychlorinated biphenyls
(PCBs), dioxins, radiation), stimulants (caffeine, nicotine), drugs and food allergens. The few
contraindications to breastfeeding include galactosaemia in the infant, psychotropic drug abuse
by the mother and active maternal tuberculosis. In the UK, HIV-positive women are advised not
to breastfeed because of a risk of transmission to the baby. This advice is not appropriate in
countries where the risks of bottle-feeding are high, especially because of the lack of clean safe
water, and outweigh the risk of HIV infection. Some therapeutic drugs are contraindicated
during lactation or require monitoring: antineoplastic drugs and radioactive substances,
retinoids, iodides, lithium, phenindione, tetracyclines, chloramphenicol and amiodarone. Drugs
commonly used by UK mothers during lactation include analgesics, antibiotics and anti-
depressants and for most of these, concentrations in breast milk are too low to cause problems.
152
The British National Formulary (BNF) has a section on safety of drugs during breastfeeding.
153,154
Several reviews have also been published concerning this topic.
Formula feeding
If mothers cannot or choose not to breastfeed, there is a range of commercially available formula
milks designed as total substitutes for breast milk during the babys first year. They are the only
safe alternatives to breast milk and infants can grow and develop normally on these feeds. The
155
content of infant formula is tightly regulated. There is an international code, legally binding in
the UK, governing its marketing, to prevent mothers from being encouraged to formula-feed
(see Appendix 5).
Formula milk has changed considerably over the past 70 years and there are frequently new
compositional changes. Standard formula is based on skimmed cows milk, with whey protein,
vegetable oil and extra vitamins and minerals added to bring the composition closer to human
milk. Formula does not contain most of the bioactive factors present in human milk, the protein
content is higher and different in quality, and the concentrations of most vitamins are higher
(see Appendix 6).
Several specific additives, which are present in breast milk but low in cows milk, have been
156, 157
introduced to some formula milks recently and may be unfamiliar to many professionals.
These include amino acids such as taurine; long-chain polyunsaturated fatty acids (LCPUFAs) such
as docosahexanoic acid (DHA); oligosaccharides; and pre-formed nucleotides. Docosahexanoic acid
is a major constituent of neuronal cell membranes and there is some evidence that newborns,
especially pre-term babies, cannot synthesise adequate quantities for optimal brain development,
although this theory is controversial. Oligosaccharides are analogous to cell surface receptors for
pathogens and are thought to inhibit the pathogenicity of bacteria. In infant formula they are

known as prebiotics (distinct from probiotics or so-called friendly bacteria, which are not currently
added to formula). Pre-formed nucleotides are thought to be required for the growth of rapidly
dividing cells in bone marrow and intestinal epithelium, and also to enhance beneficial intestinal
bacterial growth. There is currently no strong evidence that these additives have health benefits.
Complementary feeding
Complementary feeding is the term used for the introduction of foods other than milk (sometimes
called weaning foods or solids). It is recommended that complementary feeds are introduced from
the age of six months onwards, and that infants progress onto the same foods as the rest of the
family by around one year. The optimal diet for infants at this stage is not known, and is certainly not
innate knowledge for parents. Detailed guidelines are available on suitable foods at every stage
(see Appendix 4). Key recommendations are a varied diet, adequate energy density, high-quality
(preferably animal) protein sources, and fresh fruit and vegetables.
Vitamin supplements for infants

Advice in the UK is that healthy breastfed infants under six months do not require supplements
117
provided the mother has adequate vitamin status. If there is any doubt about this, supplements
should start at one month. From six months, infants receiving breast milk as their main drink should
have vitamin A and D supplements, but these are not required by infants on formula-milk, which is
fortified with vitamins. Pre-term infants are a special case and require supplements from birth.
Between one and five years, it is recommended that all children have vitamin A and D supplements
unless their diet is diverse and plentiful and there is good exposure to sunlight. There are many
152, 158
preparations available. Supplementary vitamins are available free for families receiving certain
benefits under the Healthy Start scheme, and all families can buy these preparations.
Developing country perspective on complementary feeding

Infants in developing countries are at increased risk of undernutrition after six months, when
breast milk alone is no longer nutritionally adequate but complementary foods are frequently of
3, 159 159
very low nutritional quality. The WHO has developed guidelines for infant feeding which are
suitable for use in all countries (see Appendix 4). Educational interventions and supplementation
programmes, designed to improve the quality of complementary feeding, have been shown to
123
reduce or prevent stunting in vulnerable infants.
Determinants of infant weight gain and growth

A characteristic of the healthy infant is rapid, though also rapidly decelerating, weight gain and linear
growth, but the factors which determine these processes and the relative accrual of lean and fat
body mass are still poorly understood. Given adequate postnatal nutrition, babies who experienced
intra-uterine growth restriction due to placental insufficiency, small maternal size, maternal
undernutrition or smoking tend to show catch-up weight gain and growth, while macrosomic
babies of mothers with gestational diabetes catch-down. Early postnatal growth rates therefore
160
compensate for intra-uterine restriction or enhancement of growth. Boys gain weight and grow
slightly faster than girls in early infancy. Weight gain and growth are modified by the type of feed
used. Formula-fed babies gain weight and length faster than breastfed babies after the age of three
160-162
to four months (see Figure 11). Small-for-gestational-age (SGA) babies grow faster on enriched
163
than on standard formula. Infant feeding is largely demand-driven in that mothers tend to offer
feeds when the baby appears to want them, and appetite is likely to be one of the factors
influencing weight gain. Recurrent infections are a major cause of poor infant weight gain and
growth in developing countries.

Figure 11: Mean weight and length of breastfed and formula-fed infants from birth
to 18 months
Breastfed
Formula-fed 80 Girls 12 Girls
10
70
8
Length (cm)
Weight (kg)
6
60
50 2
0 2 4 6 8 10 12 14 16 18 0 2 4 6 8 10 12 14 16 18
Age (months) Age (months)
Breastfed
Formula-fed
80 Boys 12 Boys
10
70
8
Length (cm)
Weight (kg)
6
60
50 2
0 2 4 6 8 10 12 14 16 18 0 2 4 6 8 10 12 14 16 18
Age (months) Age (months)
Source: Dewey KG, Heinig MJ, Nommsen LA et al (1992) Growth of breastfed and formula-fed infants from
0 to 18 months: the DARLING study. Pediatrics 89: 1035-41.

164
Karlberg described postnatal growth in three distinct phases infancy, childhood and puberty.
During infancy the fetal growth hormones, such as insulin and the insulin-like growth factors (IGFs)
play a more important role than growth hormone. From six to 12 months, growth hormone starts
to have a significant effect on growth and becomes the main endocrine growth regulator during
childhood. Nutritional status, especially during infancy, interacts with these hormones, and both
circulating IGF-1 concentrations and receptors are reduced in undernutrition. Thyroid hormone is
required for normal infant growth. In early infancy, gonadotrophin concentrations are high, and
testosterone concentrations in boys are raised; they fall over the first six postnatal months to very
low levels that persist until the onset of puberty. There may be mild elevation of oestrogen
concentrations in girls in the neonatal period.
The reasons for differences in weight gain and growth between breastfed and formula-fed babies
are not known. Formula milk contains more protein than breast milk, which may alter growth
factor concentrations. The greater control that the infant exerts over the flow of milk, and the
supply and demand interaction between infant and mother, may influence appetite, satiety and
energy intake differently from formula-fed babies. Inadequate growth is often a reason for
mothers deciding that they have insufficient milk, and changing to formula feeding (see pages 28
and 29). There are also numerous social factors influencing parents infant feeding choices. This
complex interplay between biological and societal influences makes it difficult to disentangle the
165
factors that control infant growth.
Key message
Inadequate growth is often a reason for mothers mistakenly deciding that they have
insufficient milk, and changing to formula feeding.
Recommendations about size and growth during infancy

Growth monitoring is one of the prime activities of health visitors and doctors looking after infants
in the UK. The aims are to detect inadequate weight gain or growth (failure to thrive), which may
indicate illness or problems with feeding or diet, or excessive weight gain. Research suggests that it
166
is important to parents that their child is normal in size or growth and a belief that an infant is
not gaining weight normally is one of the commonest reasons mothers give for stopping
breastfeeding. The growth charts currently in general use in the UK are based on the 1990 UK
167-169
reference data. These came from a study of fetal growth in white Caucasian pregnancies in
London, and Cambridge infants taking part in a study of the effects of infant feeding practices
on growth.
In 2006, the WHO launched a new growth reference, which is now recommended for use
170
worldwide. There were a number of reasons for developing the new reference. Formula-fed
162
infants gain weight more rapidly after the first four to six months than breastfed infants and
studies had shown that the weight gain pattern of breastfed infants deviated considerably from
171
most current reference data. An optimal reference was considered to be that based exclusively
on breastfed infants. Infants from all ethnic groups can grow equally well, given an optimal
environment and adequate nutrition, and a unified standard would have benefits for comparing
data from different populations. The WHO has defined the new reference as a standard rather
than a reference, ie a description of how children should grow. The infants from which it was
derived lived in conditions favourable to child growth: they were singletons born at full-term
without major neonatal morbidity; had no known health or environmental constraints to growth;

the mothers were willing to breastfeed exclusively for at least four months continuing until
12 months, and to introduce complementary feeds by six months; and none were smokers. The
data were collected using standardised techniques in the USA, Oman, Norway, Brazil, Ghana and
India in 1997-2003. One concern about the generalisability of these standards is the wide
international variation in birth weight. Mean maternal height and birth weight in Oman and India
were much lower than in Norway and the USA, indicating maternal constraint on fetal growth in
these developing countries, which is also likely to be associated with effects on postnatal growth,
172
inducing more rapid catch-up growth.
Box 9: Comment on the WHO infant growth reference standard
The most interesting thing about the study that gave rise to these standards is that despite
being based on very diverse populations around the globe, they produced very similar growth
curves, indicating that genetics plays a very small part in determining growth rates compared
with environmental factors which were optimised for this study healthy pregnancy, good
mother and child nutrition, no smoking, full breastfeeding etc.
Tim Lobstein, Director Childhood Obesity Research Programme
A joint expert group from SACN and the Royal College of Paediatrics and Child Heath (RCPCH)
172
met to consider the routine use of the WHO standards in the UK. They concluded that UK
infants would appear large at birth and show apparent marked catch-down growth during the first
few weeks, which could discourage mothers from breastfeeding. Using the WHO standards would,
however, reduce the number of UK infants showing weight faltering, and thus being classified as
underweight, after four months. They found little difference in length between the UK 1990 and
WHO references at any age, and there was convergence of weight in the two references from
around two years onwards. The group advised adoption of the WHO Growth Standard for routine
use from two weeks to 24 months, while retaining the UK 1990 reference from 24 months
onwards. Since the WHO reference population did not include pre-term infants, the UK 1990
reference would also need to be retained for these infants. They recommended piloting of the new
charts, training for health professionals, and a well-planned communications strategy preceding
implementation. It is not clear when all this will happen, but it is unlikely that the standard will be
in general use before 2009.
Key message
Infant growth-charts currently in general use in the UK (based on 1990 UK reference data) are
now considered inadequate because weight gain patterns of breastfed infants deviate
considerably from such data. Old growth charts should be replaced by the 2006 WHO new
growth reference based exclusively on breastfed babies for assessing all infants aged
between two weeks and 24 months.

Breastfeeding and health: short- and long-term outcomes

Even in developed countries, with modern breast milk substitutes and easy access to clean water for
preparation, breastfeeding is associated with fewer infections, especially gastroenteritis and respiratory
173-177 173
infection, and possibly otitis media. In one UK study, babies who were fully or partially breastfed
for 13 weeks or more were seven to 17 per cent less likely to have a gastro-intestinal illness and were
70 per cent less likely to be admitted to hospital with gastro-intestinal illness. Significant reductions in
gastro-intestinal illness in this group were found up to one year of age.
McCance and Widdowson demonstrated in animals over 40 years ago that early postnatal nutrition
178, 179
has long-term effects. They showed that by manipulating litter size at birth, rat pups could be
transiently overfed or underfed during lactation; reducing the litter size resulted in more rapid early
growth and larger adult size. Later overfeeding did not have this effect, suggesting that there is a
critical period within which postnatal nutrition permanently influences growth and body composition.
Most research into long-term effects of infant feeding in humans has compared rates of various health
outcomes between children or adults who were breastfed or formula-fed. Despite a wealth of
literature, there is still much that we do not know. The ability to combine infant feeding data with
adult outcomes means that a dataset must be quite old, dating back to when bottle feeds were very
different from those in use today. Information about feeding is usually sparse, recording whether or
not a baby was initially breastfed, and sometimes the duration of breastfeeding and/or the age at
which solids were introduced. Collating evidence across studies can be difficult because of the different
ways of describing infant feeding. There is no information in these studies on the quality and quantity
of breast or bottle milk. A major problem in interpreting these studies is that of confounding.
A mothers choice to breastfeed is related to many other factors that could influence the later health
of the child, especially her socio-economic status and education (see page 30). These influences
change with time. Adjusting for these factors, to isolate the biological effects of early feeding, is an
imperfect science.
Randomised trials would be helpful, but it is clearly impossible to randomise healthy babies to be
180
breastfed or formula-fed. A recent trial in Belarus in which mothers attending different health clinics
were randomised to receive or not receive intensive breastfeeding education and support, leading to
greatly increased rates of breastfeeding in the former group, is likely to yield useful data. Lucas and
colleagues have carried out randomised trials of different infant feeds among babies born pre-term or
SGA (see page 41). The ongoing European Childhood Obesity Project is carrying out a series of
randomised trials in babies whose mothers have decided to bottle-feed, testing the effects of different
181
protein intakes from formula milk.
Developing country perspective on breastfeeding and health

Breastfeeding is a lifesaver in developing countries, where formula feeds are often by necessity
made with unsterile water and fed from unsterile bottles and teats. A recent review estimated
relative risks for diarrhoea incidence and mortality under six months at 3.0 (95% confidence
interval (CI) 1.3 to 7.0) and 4.6 (95% CI 1.8 to 11.8) for partially breastfed infants and 3.7 (95%
CI 1.7 to 7.9) and 10.5 (95% CI 2.8 to 39.6) for non-breastfed infants, compared with exclusively
3
breastfed babies. Estimates for pneumonia incidence and mortality were 2.5 (95% CI 0.2 to 27.2)
and 2.5 (95% CI 1.0 to 6.0) in partially breastfed infants and 2.1 (95% CI 0.2 to 22.6) and
15.1 (95% CI 0.6 to 373.8) in non-breastfed infants. The same review estimated that sub-optimal
breastfeeding causes 1.4 million preventable deaths (12% of under-five deaths in developing
countries) and 43 million disability adjusted life years (DALYs).

Breastfeeding and later cognitive function and neurodevelopment

A large number of studies have compared neurodevelopmental scores and visual function between
182-184
children who were breastfed and those who were formula fed. A consistent message is that at
all ages children who were breastfed score an average two to eight developmental quotient points
higher and/or have better visual function. Several studies report dose-response effects with
duration of breastfeeding. The size of these effects is small, and unlikely to make a difference to
an individual child, although on a population scale they could be important. The issue of
confounding is especially important for cognitive outcomes, because mothers who breastfeed tend
to be more affluent and better educated than women who formula-feed. In a large recent study, it
was shown that the mothers intelligence quotient (IQ) predicted her likelihood of breastfeeding
185
even more strongly than these factors. A one standard deviation advantage in maternal IQ more
than doubled the odds of breastfeeding. Before adjustment, breastfeeding was associated with an
increase of around four points in childhood cognitive ability, but when adjusted for a range of
confounders including maternal IQ, the effect was non-significant (+0.5 points, 95% confidence
interval -0.2 to +1.2).
There are however, plausible biological reasons for better cognitive development in breastfed
babies. The close contact and interaction between mother and baby may enable more visual, social
and motor stimulation in early infancy. Constituents of breast milk could favour brain development.
The LCPUFAs, DHA and arachidonic acid (AA) are required in large quantities in the developing
brain and retina. They have not been added to formula milk until recently (~2002 onwards) and
are not present in all formulas. DHA can however, be synthesised from precursors in formula, and
there are only small differences in brain DHA content between breastfed and formula-fed infants.
It is not yet known how important these differences are in functional terms. They may be more
important in pre-term babies, since accumulation of DHA in the fetal brain occurs mainly in the
last trimester of pregnancy. Randomised studies in pre-term infants, comparing banked breast milk
with pre-term formula (both given by nasogastric tube) showed that breastfed infants had an eight
186
point IQ advantage at eight years, even after adjustment for confounding factors.
Key message
There is consistent evidence of better cognitive function in children who were breastfed.
There is controversy as to whether this is a direct effect, or the result of confounding
resulting from the fact that mothers who are more intelligent and/or better educated are
more likely to breastfeed.
Breastfeeding and later body composition and obesity

There are several recent systematic reviews of studies comparing indices of obesity between
187-190
children and adults who were breastfed or formula-fed. BMI, which does not distinguish
between fat and lean body mass, was the main outcome in most studies, but some used specific
measures of adiposity such as skinfold thickness or dual-energy x-ray absorptiometry (DXA)
measurements.
Breastfeeding is associated with a lower mean BMI in later life in most studies. The difference is
2 189 2
small (-0.04 kg/m [95% CI 0.05 to -0.02]) but the lower incidence of obesity (BMI >30 kg/m )
188
is more impressive (odds ratio [OR] 0.87 [95% CI 0.85 to 0.89]). Several studies have shown a
dose-response relationship, with longer duration of breastfeeding associated with lower rates of
obesity. Again, there are major confounding issues, because the choice to breastfeed is associated

191, 192
with less obesogenic family characteristics. A recent study showed however, that fat mass
assessed using DXA at age nine to 10 years was inversely related to the duration of breastfeeding
and this association, although attenuated, was robust to adjustment for a range of confounding
192
factors. On the other hand, there were no differences in skinfold thickness at six years of age
180
between children in the two arms of the Belarus trial.
Mechanisms that could protect breastfed babies from later obesity include aspects of the feeding
process or particular constituents of breast milk. As already mentioned, breastfed infants may learn
to regulate their energy intake more effectively. Breastfed babies grow more slowly in infancy than
formula-fed babies, which may be protective. Constituents of milk, such as protein, may influence
127, 193
body composition through effects on hormones such as insulin and IGF-1.
Key message
Breastfeeding is associated with a lower mean BMI in later life, and a longer duration of
breastfeeding is associated with lower rates of obesity. Breastfed babies grow more slowly in
infancy than formula-fed babies, which may be protective against the later development of
obesity. There is also evidence that breastfeeding is associated with a lower risk of both type 1
and type 2 diabetes and some forms of cancer, and lower LDL-cholesterol concentrations in
childhood and adulthood.
Diabetes
Type 1 diabetes is an auto-immune disease in which antibodies are formed against components of
the pancreatic beta cells, leading to insulin secretory failure. It usually presents in childhood or
adolescence. Case-control studies have shown a 30 to 50 per cent reduced risk of type 1 diabetes
in children who were breastfed, but more evidence is required in this area. It has been suggested
that the avoidance of cows milk formula is important rather than breastfeeding per se, because
there is structural similarity between bovine albumin and beta cell surface proteins, and children
194
presenting with type 1 diabetes have elevated antibodies to bovine albumin.
Type 2 diabetes is a common disease and, until recently, usually presents in middle-to-old age. It is
strongly associated with obesity, and the underlying cause is insulin resistance, which imposes an
increased demand for insulin that eventually exhausts the pancreatic beta cells. The obesity
epidemic in Western countries has led to increasing numbers of children presenting with type 2
diabetes. It has been estimated that there could be 1,400 children with type 2 diabetes and
195
20,000 with pre-diabetes (impaired glucose tolerance (IGT)) undetected in the UK. There is some
evidence that breastfeeding protects against the risk of developing type 2 diabetes in later life,
possibly through effects on adiposity. A meta-analysis of seven studies showed a reduced risk in six
196
(overall OR 0.61; 95% CI 0.44 to 0.85; p=0.003). This was little changed after adjusting for
confounding factors (maternal size, birth weight, parental diabetes, socio-economic status and
adult body size).

Blood pressure and cardiovascular disease

There were no differences in blood pressure at six years of age between children in the two arms of
180 197, 198
the Belarus trial. Two recent systematic reviews found that breastfeeding was associated with a
small reduction in blood pressure of 1-1.5 mmHg (systolic) and 0.5 mmHg (diastolic) in observational
studies. Effect estimates were lower after adjusting for confounding. Although small in individual
terms, an effect of this size at a population level could translate into significant reductions in
hypertension and CHD. A meta-analysis of the few studies that have related infant feeding to
cardiovascular disease found no evidence of a lower incidence in men and women who were
199
breastfed. There was some evidence that prolonged breastfeeding (for more than a year) was
associated with a small increase in adult cardiovascular disease mortality in this analysis, and with
200
increased arterial stiffness in one other cohort study.
Other cardiovascular risk factors

There are few data for other risk factors such as serum lipid concentrations and inflammatory markers. A
meta-analysis found that breastfed babies have higher serum cholesterol and low-density lipid (LDL)
cholesterol concentrations in infancy itself (probably because of the higher cholesterol content in breast
milk) but concentrations were lower in adult life by -0.18 mmol/l (CI -0.3 to -0.06). This difference would
201
be associated with an approximate 10 per cent reduction in CHD risk. Consistent with these findings, in
a follow up study of pre-term infants randomly assigned to banked breast milk or pre-term formula,
202
children in the former group had lower LDL cholesterol and apolipoprotein B concentrations. A recent
study of 8,000 members of the 1958 UK birth cohort, whose infant feeding was recalled by the mother
at seven years, and in which it was possible to adjust for confounding factors, showed that a longer
duration of breastfeeding was associated with lower plasma fibrinogen, plasminogen activator inhibitor
203
and von Willebrand factor, although the effects were small.
Cancer
Higher birth weight and taller adult height are associated with an increased risk of some cancers,
19
suggesting effects of nutrition in early life. This may reflect exposure to hormones promoting early
growth. A recent meta-analysis suggested reduced rates of pre-menopausal breast cancer among
women who were breastfed in infancy, but found no evidence of an effect on overall cancer incidence
204
or other specific adult cancers. There may be small reductions in some childhood cancers, including
205
acute lymphoblastic leukaemia, Hodgkins lymphoma, and neuroblastoma, but data are limited.
Allergic/atopic disease
The incidence of allergic disease in infancy and childhood (wheezy bronchitis, asthma and atopic
dermatitis or eczema) has increased recently in many Western countries including the UK. Several
studies have suggested a protective effect of breastfeeding, but systematic reviews show that the
findings are inconsistent. Infants at high risk because of a family history of allergic disease do seem to
206
benefit from exclusive breastfeeding for three to four months. Soya-based formula does not protect
against atopic disease, but there is some evidence that hydrolysed formulas are protective compared
206
with formula containing intact bovine protein.
Mental health
One of the proposed benefits of breastfeeding is increased bonding between mother and baby, and an
increased sense of security that could promote psychosocial resilience and reduce mental illness. This is
a remarkably poorly studied outcome. Fergusson found no evidence of better psychosocial adjustment
207
in adolescents who were breastfed, while another small study suggested lower anxiety levels in
208
response to parental separation in breastfed children.

Other outcomes: bone health, coeliac disease, inflammatory bowel disease

Breastfed infants, consistent with their smaller size, have lower bone mineral content (BMC) than
formula-fed infants. The calcium and phosphate content of formula has been shown to influence
209
BMC during infancy in randomised intervention studies. There are, however, no data on long-
term outcomes such as adult bone density or fracture risk.
A systematic review found consistent evidence from six case-control studies that longer duration of
breastfeeding, and breastfeeding at the time of introduction of gluten containing foods, protected
210
against the later development of coeliac disease. There is inconclusive evidence of protection
194
against inflammatory bowel disease.
Other aspects of infant diet and long-term outcomes

There are very few studies relating long-term outcomes to other aspects of infant diet, for example
effects of different formulas, the age at which solids were started, the type and quality of
complementary feeds, and the use of micronutrient supplements.
Lucas and Singhal have followed up children who took part in a series of randomised trials of
202, 211-213
different formula feeds as babies born pre-term or SGA. Among pre-terms those who
received banked breast milk had the lowest blood pressures and 32-33 split proinsulin
concentrations (an indicator of insulin resistance) at 13-16 years. Those fed enriched pre-term
formula had the highest, and those fed standard formula had intermediate levels. Term SGA babies
fed standard formula had lower diastolic blood pressures at six to eight years than those fed
enriched formula.
The macronutrient balance of the infant diet may be important. Higher protein intakes in late
193, 214
infancy have been associated with greater adiposity in childhood. Another study suggested
that animal protein (especially dairy protein), but not vegetable protein, was linked to later
215
adiposity. The INCAP trial in Guatemala, randomised villages to receive one of two supplements
for mothers and children: high-protein, high-energy drink (protein 6.4 g/100ml, energy 900 kcal/l)
or a lower nutrient drink (energy 330 kcal/l, no protein). Both contained multiple micronutrients.
People who received high-nutrient drink in utero (through their mother) and/or infancy (either
through their mothers breast milk or by direct intake) had lower adult triglyceride concentrations
95
and higher HDL cholesterol concentrations.
Evidence linking the early introduction of solid feeds to allergic disease (eczema, asthma, and
216 217, 218
others) and obesity in childhood is inconclusive.
The timing of introduction of solids and later health

It has been suggested that introducing certain foods too early or too late during infancy increases
the risk of developing food allergies and atopy (eczema and wheezing). The evidence base is not
strong. In the UK it is recommended that certain foods are never introduced before six months
(see Appendix 4).
Symptoms of food allergy and intolerance in infancy can be obvious (facial swelling, urticaria) or
non-specific (coryza, wheezing, vomiting, diarrhoea, colic, blood in the stools). The commonest
allergies are to cows milk protein, egg, soya, wheat, nuts and shellfish. Diagnosis is based on
history, skin prick testing, the measurement of food-specific IgE antibodies, patch tests, and food
219, 220
challenge testing. The latter should be carried out using a blinded format, and placebo controls.

There is little evidence that adding probiotics (live non-pathogenic bacteria that colonise the gut) or
prebiotics (nondigestible food components such as oligosaccharides that stimulate the growth of
221, 222
non-pathogenic bacteria in the gut) to infant feeds reduces later food allergy/intolerance.
Infant growth and long-term outcomes

There is strong and consistent evidence that undernutrition in infancy is associated with permanent
adverse effects on growth and development. In a recent analysis of young adults from five
developing countries, stunting and/or underweight at the age of two years were associated with
19
reduced adult height, fewer years of attained schooling and lower adult income or assets. Among
women, undernutrition in infancy was associated with lower birth weight in the next generation.
These relationships remained after adjustment for childhood socio-economic status and parental
education, suggesting that they were related to infant undernutrition, rather than simply a
reflection of continuing disadvantage in later life. A literature review also found consistent
evidence of impaired cognitive ability in children who had been undernourished (stunted or
19
wasted) in infancy.
Key message
There is strong and consistent evidence that poor weight gain and growth during infancy are
associated with permanent stunting and cognitive impairment, resulting in fewer years of
attained education, and lower adult productivity and earning capacity.
The relationship of infant size and growth to later health outcomes in well-nourished populations
is currently unclear and controversial. This is partly because of a paucity of data. Cohort studies old
enough to hold data on both infant size and adult disease are few. In a recent systematic review
relating size in infancy to the 12 diseases accounting for the highest burden of disease (ischaemic
heart disease, stroke, depression, lung cancer, road traffic accidents, alcohol abuse, dementia,
chronic obstructive lung disease, suicide, breast cancer and diabetes (split into type 1 and type 2))
223
only 19 good quality studies, relating to 10 of the disease outcomes, were found. The highest
number of studies for a single disease was seven for type 1 diabetes, a disease with its onset
mainly in childhood. Three of these seven studies showed a positive association between infant
weight or BMI and type 1 diabetes risk. This is consistent with the data described previously
showing a lower risk of type 1 diabetes in children who were breastfed (see page 42).
Several studies of cardiovascular risk factors in children have shown higher blood pressure in those
224, 225
who gained more weight during infancy. In non-randomised analyses of Lucass infant feeding
trials, SGA babies who gained more weight between birth and nine months had higher diastolic
213
blood pressure in childhood and pre-term babies who gained more weight in the first two weeks
202, 212
had higher 32-33 split proinsulin concentrations and LDL/HDL ratios at 13-16 years. Greater
weight gain in infancy is consistently associated with higher BMI, and in some but not all studies
19, 226-228
with greater adiposity, in later childhood and in adult life. These studies have led to the
229
Growth Acceleration Hypothesis, which suggests that rapid weight gain in infancy, as well as in
later childhood, is a risk factor for later cardiovascular disease.
In marked contrast to these data, retrospective studies of adult cohorts suggest benefits of infant
weight gain. In the Hertfordshire cohort, men with a higher weight at one year had lower
47, 230, 231
cardiovascular disease mortality (see Figure 12) and were less likely to have impaired
232
glucose tolerance or type 2 diabetes. Men and women in Finland who developed CHD or type 2

231, 233
diabetes were significantly lighter, thinner and shorter than average in infancy. In the New Delhi
231, 234
birth cohort in India, lower weight at one year predicted an increased risk of IGT or type 2 diabetes.
Figure 12: Cardiovascular disease mortality according to weight at one year in

Hertfordshire men
140
120
Standardised mortality ratio
100
80
60
40
20
0
-18 -19 -20 -21 -22 -23 -24 -25 -26 -27
Weight at 1 year (pounds)
Source: Osmond C, Barker DJP, Winter PD et al (1993) Early growth and death from cardiovascular disease in
women. British Medical Journal 307: 1519-24.
Two of these three adult cohort studies had data on weight and BMI gain in childhood and
233, 234
adolescence as well as in infancy. Men and women with CHD or diabetes were light and thin
as infants but gained weight more rapidly than average in later childhood (see Figure 13a and b)
suggesting that infant weight gain and childhood weight gain may have completely different
effects on later disease risk. There was no evidence that increased height at any stage of childhood
was associated with adverse outcomes in adult life. The reasons for the different findings in the
adult and childrens studies are not known. One possibility is that the rapid infant weight gain seen
in the Hertfordshire, Finland and Delhi babies reflected healthy weight gain in predominantly
breastfed babies, whereas the rapid weight gain seen in recent studies of children reflected the
effects of predominant formula feeding. Recent data suggest that breastfeeding attenuates the
235
effect of rapid infant growth on adiposity at the age of two years.
Key message
While the long-term effects of rapid weight gain in infancy require further research, there is
clear evidence that excessive weight gain in childhood and adolescence is associated with an
increased risk of adult obesity, type 2 diabetes and cardiovascular disease.

Figure 13a and 13b: Height and weight scores in infancy of individuals having CHD in
later life
Height 0.3 Boys

BMI
Z-score
Weight 0.2
0.1
COHORT
0
-0.1
-0.2
-0.3
0 6 12 18 2 4 6 8 10
Age (months) Age (years)
Height 0.3 Girls

BMI
Z-score
Weight 0.2
0.1
COHORT
0
-0.1
-0.2
-0.3
0 6 12 18 2 4 6 8 10
Age (months) Age (years)
Mean standard deviation (SD) scores for height, weight and body mass index in infancy (up to two years) and
from two to 11 years after birth among boys and girls who had CHD as adults. The dotted line at zero
represents the average for the whole cohort.
Source: Barker DJP, Osmond C, Forsen TJ et al (2005) Trajectories of growth among children who have coronary
events as adults. New England Journal of Medicine 353: 1802-9.

There is another paradox in the data from the older cohorts, which needs to be investigated. High
BMI is a risk factor for cardiovascular disease and diabetes, but the relationships of infant weight
gain to adult BMI and to adult disease are in opposite directions. The key to understanding this
may be to obtain better information about body composition in infancy. The Delhi study showed
that infant BMI gain was more strongly related to adult lean mass than to adult adiposity, while
19, 236
BMI gain in later childhood was strongly related to adult adiposity. Infant weight gain in
237
Hertfordshire was associated with taller adult height and bone mineral content, which would
also be associated with greater lean mass.
Key message
Several studies of cardiovascular risk factors in children have shown higher blood pressure in
those who gained more weight during infancy. On the other hand, studies of adults have
shown a lower risk of cardiovascular disease and type 2 diabetes in those who gained more
weight during infancy. These apparently paradoxical findings need to be investigated further.
There remain many unanswered questions. Most people would agree that normal infant weight
gain should be protected, but should it be actively promoted or should catch-up or rapid weight
gain be actively prevented? Is the answer to this question the same in all populations? And how
modifiable, in any case, is the weight gain of a healthy well-nourished and demanding infant?
These are important questions, because infancy is an accessible stage of life when optimal
nutrition could have lifelong benefits. In developing countries, paediatricians generally try to
promote catch-up weight gain and linear growth in small babies. There is good evidence that this
reduces infant mortality, improves growth and development and has lasting benefits on education
3, 125, 238
and work attainment. In more affluent countries such as the UK, getting infant nutrition
right is likely to be an important element of efforts to prevent obesity and common causes of
death and disability such as cardiovascular disease and diabetes.
Key message
Getting infant nutrition right has lasting benefits for growth and development, and is
important in the prevention of obesity and chronic disease in adult life.

Conclusions
Infants have special nutritional requirements because of their rapid growth and
development and vulnerability to infection. Optimal nutrition in infancy is essential for
normal cognitive and physical development and may protect against obesity and chronic
disease in adult life. Many parents need guidance to provide adequate nutrition for their
children at this stage of life.
Breast milk is the ideal food for babies in their first few months. Mothers need support in
order to breastfeed successfully. There is consistent evidence of better childhood cognitive
development, and a lower risk of several disease outcomes, including obesity and diabetes,
in children and adults who were breastfed rather than formula-fed. It is not known whether
these effects are causal or reflect the generally healthier lifestyles of the families whose
mothers choose to breastfeed.
The effects of the quality of complementary feeding on current and later health in countries
such as the UK are largely unknown. There are wide variations in infant size, weight gain,
linear growth and body composition. There is increasing evidence that these influence the
risk of developing obesity, diabetes, cardiovascular disease and other health outcomes in
later life.
The optimal pattern(s) of infant weight gain in order to minimise the risk of obesity,
cardiovascular disease and diabetes is however, not yet known. There is strong evidence that
undernutrition (stunting or wasting) during infancy leads to impaired adult cognitive,
physical and economic capacity, even if nutrition improves later in childhood.

Chapter 4: Influences on maternal

and infant nutrition and
opportunities for intervention
Interventions in maternal and infant nutrition a global perspective
239
In May 2004, WHO published a report, Global strategy on diet, physical activity and health
which stated that A life-course perspective is essential for the prevention and control of non-
communicable diseases. This approach starts with maternal health and prenatal nutrition,
pregnancy outcomes, exclusive breastfeeding for six months, and child and adolescent health.
It reaches children at schools, adults at worksites and other settings, and the elderly and
encourages a healthy diet and regular physical activity from youth into old age. This was followed
240
by the WHO report Promoting optimal fetal development: report of a technical consultation.
Its recommendations included initiatives to:
prolong the interval between menarche and first pregnancy (> four years)
improve maternal nutrition prior to conception (BMI and micronutrient status)
optimise weight gain and nutrition during pregnancy
reduce malaria, HIV and smoking
promote breastfeeding
develop strategies to avoid gross mismatch between the developmental environment and
childhood nutritional environment.
In March 2006, the World Bank produced a report entitled Repositioning nutrition as central to
124
development, which stated The emphasis of any programmes to combat poor nutrition should
target pregnant women and children under two years of age. This formed part of the World
Banks attempt to calculate the cost of a poor start to life. This was based on the savings gained
from moving an infant from a low birth weight (<2500g) to a normal (>2500g) category, under
the headings of:
reduced infant mortality
reduced neonatal care
reduced costs of infant/child illness
productivity gain from reduced stunting
productivity gain from increased ability
reduction in costs of chronic diseases
intergenerational benefits.
The total saving was $510 (US) for each low birth weight prevented. This is recognised to be an
under-estimate and work is now ongoing to amend it to take into account newer perceptions.
Additional factors that may increase the estimate include the fact that the risk of non-
communicable disease is graded across the normal birth weight range and is not just a
consequence of birth weight below 2500g, and that disease risk is also associated with high
birthweight. Chronic non-communicable diseases now start earlier in life in many populations and
the effects can be passed across more than one generation. The discount model, which assesses
the relative saving on later poor health by investing in preventative measures, may be too simple
for calculating the real cost-benefit relation. Notwithstanding the need to obtain new estimates of
the cost, influential economists agree that human development offers a very important time over
241
which to intervene to promote later health.
Interventions designed to improve short-term outcomes

Many trials have tested the effect of nutritional supplementation in the mother (usually started in
mid-late pregnancy) on birth weight. Few have assessed the effect of pre-conceptional
supplementation on fetal growth but there are ongoing trials aimed at doing this. In an early trial
in the Gambia, a high-energy biscuit for severely undernourished pregnant women increased birth
weight by more than 130g, but most trials of energy and protein supplementation have shown
8
only small increases in birth weight (around 50g overall). The same is true of multiple

9
micronutrient supplementation trials. Birth weight is a crude measure of fetal development, and
may under-estimate effects on specific fetal tissues and organs. The Gambia high-energy biscuit
trial, and a recent trial of multiple micronutrient supplementation in Indonesian mothers, reported
242 243
reduced infant mortality but opposing results were found in two earlier trials in Nepal. More
measurements of functional outcomes such as growth and risk factors for later disease are
required in such trials.
Developing country perspective

The BMA report Improving the health of the worlds poor (2007), highlights the persisting
problems of poverty and undernutrition in many developing countries and its effects on
maternal, fetal and infant health. Young women often have little control over family finances
and food purchases, and come last in the family hierarchy in terms of access to food. Babies
born to undernourished women are more likely to be born pre-term and/or be growth
restricted. Sub-optimal breastfeeding practices and poor-quality complementary feeding
frequently follow and set the infant on course to becoming a stunted child, with impaired
physical development and cognitive ability. An especially adverse situation, in terms of adult
health, comes from poor nutrition in early life followed by obesity in later life. This
combination is increasingly common in developing countries and carries a high risk of adult
19
hypertension, diabetes and cardiovascular disease. Of the eight United Nations Millennium
Development Goals, Numbers 1 (Eradicate extreme poverty and hunger), 4 (Reduce child
mortality) and 5 (Improve maternal health) directly relate to the issues discussed in this report.
In addition Number 2 (Achieve universal primary education), and 3 (promote gender equality
and empower women) are related goals. While progress towards these is being made, it is
likely that many of them will not be met by the target year of 2015.
Guidelines for improving the diets of young women in the UK

There have been consistent dietary messages to adults over many years to encourage consumption
of fruit and vegetables, starchy foods and oily fish, and to limit consumption of dietary fat, salt and
added sugar. The recommendations for a healthy diet were based on evidence of the role of diet
244, 245
in the aetiology of cardiovascular disease and some cancers, and recently specific advice on
246-248
oily fish consumption, salt and vitamin D intakes has been updated. Dietary guidelines are
comparable across the developed world. Current UK advice is depicted in the Eatwell plate
249
model. While this advice may be widely understood, the most recent National Diet and Nutrition
Survey (NDNS) shows that many adults do not comply with these dietary guidelines, and that the
2, 250, 251
diets of young adults may be a particular cause for concern (see Box 10).

Box 10: The diets of young people: findings from the National diet and nutrition survey
When compared with older adults, young men and women in the NDNS were more likely to
consume fast foods, savoury snacks, and carbonated soft drinks, and less likely to eat
wholemeal bread, whole grain cereals and oily fish.
Although fruit and vegetable consumption was below the target of five daily servings for
many adults, consumption was particularly low among young adults (1.3 and 1.6 servings
per day in men and women aged 19 to 24 years respectively).
In comparison with older age groups in the NDNS, younger men and women obtained the
largest proportion of food energy from non-milk extrinsic sugars and had the lowest intakes
of dietary fibre (non-starch polysaccharides), vitamin A, riboflavin, folate, vitamin D, iron,
calcium, magnesium and zinc.
These findings show that poor quality diets are common among young people in the UK raising
the possibility that, for many young women, current patterns of diet and nutritional status could
impact on their ability to meet the nutrient needs of future pregnancies.
There are currently few specific dietary recommendations for pregnancy (see Appendix 3). The
most consistent dietary message to pregnant women in the UK is to increase folate intake before
conception, and recent data show widespread awareness of the need for adequate folate status in
131
pregnancy. Among mothers studied in the Health survey for England in 2002 who had planned
their pregnancy, more than half (55%) reported taking dietary supplements or changing their diet
prior to pregnancy to increase folate intake. Of mothers who increased their folate intake before
conception, 61 per cent reported that they had done so at least three months before becoming
pregnant. Use of folic acid supplements was uneven, however, and was less common among
women of lower social status. The value of recommendations for preconception supplementation
252
with folic acid may be limited due to the high rates of unplanned pregnancies in the UK.
Key message
Poor quality diets are common among young people in the UK raising the possibility that,
for many young women, current patterns of diet and nutritional status could impact on their
ability to meet the nutrient needs of future pregnancies.
Apart from these specific recommendations for pregnancy, young women are encouraged to
comply with general healthy eating advice before and during pregnancy. Given that so many
young women do not follow current guidance, it is clear that it is not sufficient just to popularise
dietary messages. To achieve change in dietary behaviours, the influences on food choice need to
be considered and understood.

Influences on food choices in women

A vast array of factors influence food choice. They include cultural, social and environmental factors,
as well as knowledge and understanding of the role of food in health and disease. In a recent study
of 6,125 women aged 20 to 34 years living in Southampton, compliance with current healthy
139
eating recommendations was described using a score for a prudent dietary pattern. Women with
high scores had diets characterised by a high consumption of fruits, vegetables and wholemeal
bread while women with low scores had diets characterised by a high consumption of white bread
and chips, added sugar and full-fat dairy products. The most important influence on the prudent
diet score was the educational attainment of the woman, such that lower scores were much more
common among women with few educational qualifications (see Figure 14). This influence was far
more important than any other factor considered, including the womans social class, the
deprivation score of her neighbourhood, or whether she was in receipt of financial benefits.
Figure 14: Percentage of women with prudent diet scores in lowest quarter of distribution,
according to their educational attainment: 6,125 women in the Southampton Womens Survey
60
Proportion with low prudent diet score (%)
50
40
30
20
10
none CSE O-level A-level HND degree
Source: Robinson S, Crozier SR, Borland SE et al (2004) Impact of educational attainment on the quality of
young womens diets. European Journal of Clinical Nutrition 58: 1174-80.
253
Although cost is a recognised barrier to eating healthily the less prudent diets observed in this
study did not seem to be simply a result of lower income.
The relationship between income and diet is complex. The low income diet and nutrition survey
(LIDNS) published in 2007 yielded a positive view of the diets of people living on low incomes in
the UK, since in comparison with the general population, the types and quantities of many foods
254
eaten and patterns of nutrient intake were similar. Consumption of fruit and vegetables by low-
income participants however, was lower, and consumption of soft drinks, processed meats, whole
milk and sugar was greater. Food security was also assessed in this study; 39 per cent of the low-
income population reported that they had been worried that their food would run out before they
got money to buy more in the past year and 36 per cent said that they could not afford to eat

balanced meals. Although the diets of children in food insecure households were comparable with
those of children in food secure households, this was not the case for women. Women in food
insecure households had typically less healthy diets, with lower consumption of fruit, wholemeal
255
bread, meat and meat dishes and fish and fish dishes. Drewnowski and Specter describe an
inverse relationship between the energy density of foods and energy cost so that high-fat
energy-dense diets may be more affordable than prudent diets based on lean meats, fish and fresh
fruit and vegetables. This may partly explain the link between food insecurity and greater levels of
256
obesity observed in some studies, particularly among women.
Key message
Educational attainment is a key influence on the quality of young womens diets.
While a number of studies have examined the associations between diet and socio-demographic
factors, there are important environmental and contextual influences on food choice that are less
commonly considered. These include:
the effects of the physical environment, such as the distance between home and shops that may
determine the accessibility and affordability of foods, and the ability to store and cook food at home
the nature of the contexts within which food is bought and eaten that may impact directly on
purchasing patterns and foods consumed
structural differences in families and households that define the nature of shared meals
the wider influences of food advertising and the promotion of foods.
Increases in fruit and vegetable consumption have been observed following the building of new
257
superstores in areas of poor retail provision, and purchasing patterns of confectionery can be
258
changed by altering its location in a cafeteria. Interventions to change aspects of the food
environment, so that consumers are encouraged to choose healthier foods, may offer important
opportunities to achieve change in eating habits.
The choice of foods eaten is influenced by individual factors. Some of these have been extensively
researched with a view to predicting and understanding food choices. They include variations in
personal taste preferences, differences in knowledge, attitudes and beliefs as well as psychological
factors such as matters of control and self-esteem.
There are complex interactions between socio-demographic, environmental and individual influences
that act to determine food choice and these influences must also underlie the reasons why current
dietary recommendations are not met. To address the dietary and nutritional inequalities that exist
across the general population we need to identify the primary influences on food choice. With this
understanding, effective interventions can be defined to achieve dietary change.

Interventions to improve maternal nutrition
Box 11: Comment on nutritional intervention in women living in poverty
In the UK the health and wellbeing of millions of women are

influenced by living in poverty. Food choices, dietary intake and
feeding behaviour are far from optimal among poorer women,
and this situation is reflected in higher rates of diet-related
morbidity and mortality well beyond maternal and child health
considerations. Interventions to change diet need to take account
of the factors that influence household economic status and
should be integrated at policy, community and individual level.
There is a dearth of research on effective interventions in this

subgroup of the population from within the UK, although there
are some encouraging United States (US) examples to draw on
in terms of possible intervention approaches.
Lack of evidence does not mean that policy work should be

delayed. It is recognised that engaging with hard to reach
groups of women is a challenge for intervention implementation
and evaluation, and it is essential that policy work should be
evaluated for its ability to engage with target groups as well as
259
for behavioural change and health outcomes.
Professor Annie Anderson, Professor of Food Chioce
University of Dundee (2007)
A systematic review of interventions that aimed to improve diet in women who were pregnant or
of childbearing age suggested that interventions that included elements of education or
260
counselling, support and empowerment can improve nutrition knowledge and behaviour. Much
of the existing evidence on interventions to improve maternal nutrition comes from evaluation of
the federally funded US health programmes. These include the US Special Supplemental Nutrition
Programme for Women, Infants and Children (WIC) and the Expanded Food and Nutrition
Education Programme (EFNEP) both of which focus on people from disadvantaged backgrounds.
Evaluation suggests that the WIC programme which combines food supplementation, nutrition
counselling and referral to health and social services, can lead to improvement in maternal diet
261
during pregnancy, increased maternal weight gain and increased breastfeeding rates.
262
WIC programmes have also been effective at increasing fruit and vegetable consumption.
EFNEP, which aims to give low-income families food knowledge and skills and to bring about
dietary behaviour change through practical sessions delivered by peers, has been shown to
263
improve food practices among recipients. Evaluation of smaller-scale intervention programmes
within the UK has also suggested that imparting food knowledge and skills to women from
disadvantaged backgrounds has the potential to improve diet in this group. The Cookwell project,
set in eight urban communities in Scotland aims to improve diet in areas of social deprivation by
delivering food skills sessions each week over a seven-week period: in a study of 113 adults living
in areas of social deprivation, 88 per cent of whom were women, the intervention led to early
increases in fruit consumption and at six months follow-up there was a significant increase in the
proportion of subjects who reported confidence in following recipes and cooking from basic
264
ingredients.

Key messages
US programmes which combine food supplementation, nutrition counselling, cookery skills

and referral to health and social services, can lead to an improvement in maternal diet during
pregnancy and to increased breastfeeding rates.
Two recent systematic reviews have considered the effectiveness of interventions which aim to
increase fruit and vegetable consumption in adults and the findings of both have relevance for
women of childbearing age. The first focused on community interventions that were effective in
265
increasing fruit and vegetable consumption in people aged four years and over. Fifteen studies,
all of which were based in the USA, were included in the review. Four trials were specifically
targeted at parents with young children. The most effective interventions gave clear messages
about the benefits of fruit and vegetables, were intensive and used multiple strategies delivered
over a prolonged period of time, and involved families as a group in the intervention. The second,
and more recent, systematic review collated evidence from the published and grey literature
266
relating to programmes that promote fruit and vegetable consumption in adults. Forty-four
studies were reviewed, with over 70 per cent set in the USA and around 16 per cent in Europe.
Consistent positive effects were seen in studies involving face-to-face education or counselling.
A more recent US intervention study of 269 adults from low-income backgrounds evaluated the
impact of the Sisters in health nutrition education programme which aimed to increase fruit and
267
vegetable consumption among low-income groups. The intervention, which involved peer-led
small group sessions to teach cooking skills and provide social support, led to significant
improvements in fruit and vegetable intake at the end of the intervention programme.
Key message
There is limited evidence of interventions that are effective in improving maternal nutrition.
There is, however, some evidence that interventions that include elements of education or
counselling can bring about improvements in nutrition knowledge and behaviour.
Improving breastfeeding initiation and increasing duration

of breastfeeding
Women surveyed in the most recent IFS were asked about their experience of breastfeeding;
73 per cent of the women who initiated breastfeeding, but who gave up in the survey period, said
131
that they would have preferred to have continued to breastfeed for longer. The most common
reason given for stopping breastfeeding was insufficient milk. Stopping breastfeeding within two
weeks of birth was associated with rejection of the breast, or painful breasts; in later months,
returning to work or college was also associated with stopping breastfeeding.
Interventions that educate women about the benefits and practice of breastfeeding are effective at
increasing breastfeeding initiation. A recent Cochrane systematic review of seven randomised
controlled trials (RCTs) of 1,388 women demonstrated that interventions based on one-to-one
268
health education and support are effective at increasing initiation rates. Overall, the relative
likelihood of breastfeeding initiation was 1.59 (95% CI 1.25 to 1.88) in the group who received
educational interventions compared with those who received routine care. A further systematic
review based on non-randomised controlled trials as well as RCTs has suggested that peer support

may be effective in improving breastfeeding initiation rates in women from disadvantaged

261
backgrounds. One community-based controlled trial, considered in the review, was carried out
over a two-year period in two socially deprived communities in Glasgow, Scotland. One of the
communities received peer counselling from trained lay breastfeeding counsellors who were
resident within the community. A second trial set in Chicago, USA evaluated the effectiveness of a
hospital-based breastfeeding peer counsellor programme delivered to women who expressed an
interest in breastfeeding. Both studies demonstrated improved initiation rates in women who had
expressed an interest in breastfeeding, suggesting that peer-counselling programmes can be
effective at encouraging women who would like to breastfeed to follow through with their decision.
There is also good evidence that appropriate support for breastfeeding mothers can prolong the
duration of breastfeeding. A Cochrane systematic review updated in November 2006, based on
34 trials of 29,385 mother-infant pairs, showed that all forms of extra support together were
associated with an increase in duration of any (includes partial and exclusive) breastfeeding the
269
relative likelihood of stopping breastfeeding before six months was 0.91 (95% CI 0.86 to 0.96).
Additional professional support (over and above standard care) was effective in prolonging any
breastfeeding but its effect on exclusive breastfeeding was unclear. Additional support from trained
lay people was effective in prolonging exclusive breastfeeding while its effect on duration of any
breastfeeding was unclear. Exclusive breastfeeding was significantly prolonged with use of
WHO/United Nations Childrens Fund (UNICEF) Baby Friendly Hospital Initiative training for
professionals. Overall, the relative likelihood of stopping exclusive breastfeeding during the study
period considered was 0.69 (95% CI 0.52 to 0.91) in the six RCTs using the WHO/UNICEF training.
Key message
Interventions that educate women about the benefits and practice of breastfeeding are
effective at increasing breastfeeding initiation. Appropriate support for breastfeeding mothers
can prolong the duration of breastfeeding.
The WHO/UNICEF Baby Friendly Hospital Initiative

The Baby Friendly Hospital Initiative is a worldwide programme of the WHO and UNICEF. It was
launched in 1992 to encourage maternity hospitals to implement the Ten steps to successful
breastfeeding (see Box 12) and to practise in accordance with the International Code of Marketing
of Breast Milk Substitutes (Appendix 5).
Hospitals are encouraged to introduce a breastfeeding policy, educate staff to implement the policy
according to role and introduce practices which promote, protect and support breastfeeding.
External assessment can then lead to accreditation for those facilities implementing the standards
effectively. In the UK, the Initiative has been expanded to include community healthcare facilities.
Accreditation of universities which introduce approved education for breastfeeding into their pre-
registration courses for midwives and health visitors has also been introduced.

Key message
Baby Friendly accredited programmes worldwide encourage hospitals and community

healthcare facilities to promote breastfeeding and provide the training for healthcare
practitioners. They have been shown to prolong exclusive breastfeeding. NICE guidance
recommends that the WHO/UNICEF Baby Friendly Hospital Initiative should be implemented as
routine practice.
Data from the Millennium Cohort Study of 18,819 children born in the year 2000 found that
mothers delivering in Baby Friendly accredited hospitals are 10 per cent more likely to initiate
breastfeeding (after adjustment for confounding variables) than those who deliver in non-
accredited units. The study found that Baby Friendly hospital accreditation is not associated with
270
an increase in breastfeeding at one month of age.
Data on all babies (n=464,246) born between 1995 and 2002 in Scottish maternity units with
more than 50 births per year show that babies born in Baby Friendly hospitals are 28 per cent
more likely to be exclusively breastfed at seven days postnatal age than babies born in other
hospitals. Breastfeeding rates increased faster in the Baby Friendly hospitals: an 11.39 per cent
271
(95% 10.35 to 12.43) rise compared with 7.97 per cent (95% 7.21to 8.73) in other units.
A cluster randomised controlled trial among 17,046 mother-infant pairs in Belarus found that
implementing the Baby Friendly Hospital Initiative significantly increased the duration and exclusivity of
breastfeeding and decreased the risk of gastro-intestinal tract infection and of atopic eczema in the
first year of life. Infants from Baby Friendly hospitals were significantly more likely than control infants
to be breastfed to any degree at 12 months (19.7% vs 11.4%; adjusted OR 0.47; 95% CI 0.32, 0.69),
were more likely to be exclusively breastfed at three months (43.3% vs 6.4%; P<.001) and at six
months (7.9% vs 0.6%; P =.01), and had a significant reduction in the risk of one or more
gastro-intestinal tract infections (OR, 0.60; 95% CI, 0.40 to 0.91) and of atopic eczema (OR, 0.54;
272
95% CI, 0.31 to 0.95).

Box 12: Ten steps to successful breastfeeding
1. Have a written breastfeeding policy that is routinely communicated to all healthcare staff
2. Train all health care staff in the skills necessary to implement this policy
3. Inform all pregnant women about the benefits and management of breastfeeding
4. Help mothers initiate breastfeeding soon after birth
5. Show mothers how to breastfeed and how to maintain lactation if they are separated
from their infants
6. Give newborn infants no food or drink other than breast milk unless medically indicated
7. Practice rooming-in and allow mothers and infants to stay together 24 hours a day
8. Encourage breastfeeding on demand
9. Give no artificial teats or pacifiers (also called dummies or soothers) to breastfeeding infants
10. Foster the establishment of breastfeeding support groups and refer others to them on
discharge from the hospital or clinic.
Source: www.babyfriendly.org.uk
Doctors role in supporting breastfeeding

In common with all other health professional groups in the UK, doctors require education to
enable them to implement the WHO/UNICEF standards effectively. Paediatricians and obstetricians
require an understanding of the role of breastfeeding in improving the health of mothers and
babies. Paediatricians also require an understanding of the normal neonatal adaptation to
intermittent feeding after delivery, how poor practice can lead to excessive weight loss in breastfed
babies and how this can be avoided, and how to protect safety and breastfeeding when caring for
babies who are reluctant to feed after delivery or who are jaundiced or at risk of hypoglycaemia. It
is recognised that in the UK hospital doctors are not the primary caregivers for breastfeeding and
therefore it is not considered necessary for their education to include clinical skills in supporting
breastfeeding.
The requirement to educate general practitioners (GPs) to implement the breastfeeding policy has been
a source of confusion ever since the initiative was launched. GPs in the UK have a limited role in
supporting breastfeeding. Their role requires them to have a basic understanding of how breastfeeding
works, a knowledge of how to treat common breast conditions (mastitis, thrush etc), access a reliable
reference source for prescribing drugs for breastfeeding mothers and refer mothers to the most
appropriate professional for breastfeeding help and support (particularly when a baby is failing to thrive).
Key message
GPs can have a significant effect on whether or not mothers give up breastfeeding when
experiencing health problems. Baby Friendly programmes show GPs how they can support the
continuation of breastfeeding in such circumstances.

Teaching packs for Paediatricians and GPs are available from the UNICEF UK Baby Friendly Initiative
www.babyfriendly.org.uk
NICE Guidance on Breastfeeding

Recent guidance from the NICE gives evidence-based recommendations relating to the promotion
177
of breastfeeding initiation and duration. The guidance was formulated through the integration of
published scientific literature with practitioner expertise and experience obtained during a national
consultation exercise with professionals working in areas that could have an impact on maternal
and child nutrition. These included hospitals, primary care trusts and social services. The
consultation exercise focused on areas of deprivation. The guidance recommends that the
WHO/UNICEF UK Baby Friendly Initiative should be implemented as routine practice. An
appropriate range of educational and support programmes should be routinely delivered by health
professionals and peer supporters. These include antenatal breastfeeding education combined with
peer support programmes to increase breastfeeding initiation and duration among women from
disadvantaged backgrounds. Other recommendations include avoidance of routine hospital
practices that might lead to separation of mother and infant since these have been shown to be
harmful to breastfeeding rates. The guidance also states the importance of encouraging mothers
to breastfeed on demand in order to encourage breast milk production and prevent breast
engorgement and mastitis. Early skin-to-skin contact has also been shown to be effective in
increasing the initiation and duration of breastfeeding. A Cochrane review updated in 2007,
273
considered the findings of 30 studies of 1,925 mother-infant pairs. Early skin-to-skin contact had
positive effects on breastfeeding initiation (odds ratio of initiation was 1.82, 95% CI 1.08 to 3.07)
and breastfeeding duration (weighted mean difference in duration was 42.55 days,
95% CI 1.69 to 86.79).
Support for breastfeeding mothers returning to work

In the UK the proportion of women in employment has increased considerably in recent years and
about 50 per cent of women with pre-school children are in paid work outside the home. Working
mothers often return to work early after having a baby and can have difficulty maintaining
breastfeeding if not supported by their employers. This may discourage working mothers from
breastfeeding at all. Recent findings from the Millennium cohort study demonstrated that women
who were employed full-time were less likely to initiate breastfeeding than mothers who were not
274
employed rate ratio was 0.92 (95% CI 0.89 to 0.96) after adjustment for confounding factors.
Strategies to support working mothers to continue with breastfeeding are needed. A recent
Cochrane review to identify workplace interventions to promote breastfeeding, found no published
275
RCTs of relevance. This represents an important gap in the evidence given the rapid increase in
maternal employment in recent years.
Key message
Strategies are needed to support working mothers to continue with breastfeeding.
Interventions that educate women about the benefits and practice of breastfeeding and that
promote baby friendly policy and practice are effective at promoting the initiation and prolonging
the duration of breastfeeding. There are still some important gaps in the evidence, however, and
studies are needed to look for effective ways of supporting breastfeeding in the workplace.

Interventions in complementary feeding

There is little evidence relating to interventions that aim to influence the timing and nutritional
content of complementary feeding in developed country settings. One study of WIC participants
suggested that peer-delivered educational interventions can be effective in reducing inappropriate
276
early introduction of solid foods. The study was based on 181 adolescent mothers who were
shown a videotape made by a peer-group of black adolescent mothers which challenged the
barriers to following infant feeding guidance. The intervention was delivered as part of a home-
visiting programme and assessed in a RCT. Mothers who were part of the intervention group were
significantly more likely to introduce their babies to solid foods later and were more likely to report
accurate knowledge of the optimal timing for the introduction of complementary food. A recent
RCT set in Germany assessed the effect on infant diet of dietary counselling derived from food-
277
based guidelines for infant nutrition. The study found that more intensive telephone counselling
was more effective than less intensive counselling or written information alone in improving
adherence to infant feeding guidance (assessed by food-based and meal-based dietary scores). The
authors suggested that face-to-face counselling may have even greater positive effects on infant
feeding practices. In developing countries where tackling infant undernutrition is the primary focus
of intervention, there is evidence that educational interventions, combined with food support in
123
countries that are food insecure are effective in improving infant nutrient intake and growth.
Mechanisms to address nutritional inequalities in the UK

Inequalities in the nutrition of young women and their children in the UK (see Box 13) can have
long-term health consequences. Although evidence of successful interventions to address these
inequalities may be limited, we already have a sufficiently clear understanding of the effects of
early disadvantage to make the nutritional needs of mothers and their children a priority.
Box 13: Inequalities in maternal and infant nutrition
Women of lower educational attainment are more likely to have diets of poor quality than
139
other women.
Consumption of fruit and vegetables is lower in low income groups in the UK while
254
consumption of soft drinks, processed meats, whole milk and sugar is higher.
Many people with low incomes in the UK are food insecure, and food insecurity in women
254
is associated with poorer diets.
131
Breastfeeding rates are lower in mothers from disadvantaged backgrounds.
Early introduction of solids is more common in young mothers and mothers of lower
131
socio-economic status.
Compliance with infant feeding guidance to provide a diet based on fruits, vegetables and
138
home-prepared foods is strongly associated with the quality of the mothers own diet.

NICE guidance
National policy will influence the nutrition of women of childbearing age and their children. Recent
public health programme guidance from NICE on maternal and child nutrition endorses existing
278
policy on nutritional recommendations for pregnant and pre-pregnant women and for infants.
The guidance strongly reinforces and builds on the previous evidence-based guidance from NICE
177
on the promotion of breastfeeding, and recommends that all staff involved in the care of
pregnant or breastfeeding women have the appropriate knowledge and skills to support and
advise women about breastfeeding. Recent cross-government policy to tackle obesity also
highlights the importance of breastfeeding and improved childhood nutrition in the prevention
279
of obesity.
Healthy Start schemes

National programmes introduced within the UK to address inequalities in the health of young
women and children may have an important impact on nutrition. The Healthy Start scheme was
introduced in 2005, following a review of the Welfare Foods Scheme in 2000 by the Committee
on Medical Aspects of Food and Nutrition (COMA). The review recommended that pregnant
women should be given vouchers for a wider range of foods, and identified the need for health
professionals to give general dietary advice during pregnancy, emphasising the importance of
breastfeeding. The aim of Healthy Start is to reduce inequalities in nutrition for women and
children. The scheme provides food support, professional advice and support to pregnant women
and mothers of young babies and children from disadvantaged backgrounds. Like the Welfare
Foods Scheme before it, food support comes in the form of vouchers to buy milk and infant
formula and provision of vitamin supplements. As recommended by COMA, however, there is
greater flexibility within the Healthy Start scheme allowing the vouchers to be used to buy fruit
and vegetables. Early evaluation of the scheme in Devon and Cornwall suggested that women
who were recipients of Healthy Start were buying more fruit and vegetables than they were before
280
the scheme began. Further follow-up will be needed to confirm whether these beneficial effects
on fruit and vegetable uptake are observed on a wider scale and maintained in the longer term.
The evaluation did not examine overall uptake of the scheme nor were any nutritional outcomes
measured. A survey of health professionals was also carried out: interviews with a small sample of
health visitors and midwives suggested that most professionals interviewed were aware of the
scheme and how to apply it. Knowledge about some elements of the scheme remained low,
however, and the authors of the evaluation concluded that coverage of training to prepare for
Healthy Start had been somewhat patchy. Evaluation at national level is needed to assess uptake of
the scheme and to examine its impact on the nutrition of women and young children. Other public
health programmes that are directed at families with young children including Sure Start Childrens
Centres, also have the potential to bring about improvements in maternal nutrition and infant
feeding practices.
Although national policy may influence maternal and child nutrition, the central importance of the
family should also be recognised. A womans diet before and during pregnancy, and her views on
breastfeeding and weaning will be influenced by her partner, friends and family. Clear and
consistent guidance for families on the benefits of healthy eating is needed, particularly to explain
the long-term consequences for their children of early diet and nutrition. In the future it needs to
be ensured that all professionals who care for pregnant women and their families have appropriate
knowledge and skills to provide this guidance.

Tackling the problem of obesity

The DH has set targets to address obesity. The public service agreement (PSA), established in 2007
has the aim by 2020 we will have reduced the proportion of overweight and obese children to
14
2000 levels. The Government Office for Science through the Foresight programme has developed
18
a strategic approach to address the problem.
In terms of chronic disease prevention, it appears that addressing infant nutrition could impact on
these relatively short-term targets, and it would be very important in influencing the incidence of
chronic disease in the longer term. Some research shows that weight gain even in the first few
226, 227, 281
weeks of life is related to childhood obesity.
The BMA policy report Preventing childhood obesity (2005) raises concerns at the rising levels of
282
childhood obesity and poor nutritional quality of diets of children and adolescents. The report
discusses those factors contributing to the rise in obesity and highlights the responsibilities of
individuals in addressing obesity, and of policy makers to provide an environment which is less
obesogenic. The importance of infant feeding is noted and the protective effect of breastfeeding
on childhood obesity is discussed. A primary theme of this work focuses on enabling parents and
carers, as well as children, to make healthy choices through effective education and information
provision which is consistent and free from adverse influences which encourage unhealthy food
choices. Recent follow up work to this report has concentrated on:
improving school food and food education in school
lobbying for restrictions on the advertising of foods high in fat, salt and sugar to children
supporting and encouraging adoption of traffic light front-of-pack signposting.
The Foresight project Tackling obesities: future choices was announced in 2005. The BMA was a
key stakeholder and had an input particularly focused on systems mapping and scenario building.
283
The outcomes report was published in October 2007 and examines the scientific evidence base
from across a wide range of disciplines in order to understand the relationships and importance of
key factors influencing obesity. Using this evidence it aims to identify effective interventions,
predict how obesity might change in the future and identify the most effective responses. As well
as the final report, this project produced a series of reviews of the current science and models for
future trends of obesity and policy options and the impacts on health.
The Foresight report argued for a life-course approach to prevention and emphasised that society
would have to be prepared to measure success over longer timeframes than currently. A specific
recommendation was the promotion and implementation of a programme of early interventions at
birth or in infancy.
Key message
Improving infant nutrition could be very important in influencing the incidence of chronic
disease in the longer term.

Box 14: Governments obesity strategy
In January 2008, the Cross-Government Obesity Unit published its strategy for England, to
address the rising prevalence of obesity. This strategy recognises the importance of promoting
childrens health and wellbeing. It encompasses a range of recommendations that include
promotion of breastfeeding, further investment in the Healthy Schools Programme, and the
promotion of a culture of healthy eating. Through the development of a Healthy Food Code
of Good Practice, the Government aims to work with industry and other stakeholders to
develop a single approach to food labelling, to rebalance the advertising and marketing of
foods that are high in fat, salt or sugar to children, and to promote the consumption of
healthy foods, particularly fruit and vegetables. As part of the Code, all food businesses will
work with the Foods Standards Agency (FSA), DH and other stakeholders to deliver a single set
of key healthy eating messages.
In November 2007, the BMA hosted a stakeholder event on food labelling. Invited representatives
from health-related organisations and the food industry came together to discuss ways in which
healthy eating messages can be reinforced through advice about nutrition and food labelling. The
group agreed a position statement, which is available on the BMA website, (see Box 15).
Box 15: A BMA food labelling statement

January 2008
The British Medical Association (BMA) has a long-term interest in the health of the public and
believes that the increase in the frequency of obesity is a cause for great concern. While
tackling obesity requires commitment to a multi-faceted approach, there is a particular need to
change dietary behaviour. The BMA considers improved and consistent food labelling to be an
important mechanism for enabling consumers to make informed dietary choices.
The BMA believes that the food and drink industry should implement a standardised,
consistent approach to food labelling. This approach should be based upon the traffic light
front of pack labelling recommended by the FSA. In order to increase the nutritional
information available to consumers we propose that the labelling should also include
Guideline Daily Amount (GDA) information.
The BMA also recognises that public awareness should be raised about the health benefits of
micronutrients. This could be done in the form of in-store leaflets explaining the benefits of
healthy food choices and stating which foods are rich in which micronutrients.

Conclusions
Many young women have diets of poor quality and inadequate nutritional status. Less
healthy diets are more common among women of low educational attainment, and among
women who have low income and who are food insecure. Although evidence of effective
interventions to improve the diets of young women is limited, this does not mean that the
goal should not be pursued vigorously. Both nutrition education and counselling have been
shown to improve womens nutrition knowledge and behaviour.
Breastfeeding rates are low in the UK, and it is less common among disadvantaged women.
Interventions that educate women about the benefits and practice of breastfeeding, and
that promote baby friendly policies and practice, are effective at promoting the initiation
and prolonging the duration of breastfeeding.
Current studies of complementary feeding show wide variations in practice in the UK.
There are few studies of interventions to influence the timing and nutritional content of
complementary feeding in developed countries.
Infant diet is strongly linked to mothers diet suggesting that interventions to improve the
diets of young women will also have direct consequences for childrens diets.
Effective interventions are needed to improve the nutrition of young women of childbearing
age. Such interventions may influence the way in which mothers feed their children as well
as influencing the diets of women themselves. They will therefore have beneficial health
effects across generations.
Efforts to encourage the initiation and to prolong the duration of breastfeeding need to
continue and be extended. The ten steps to successful breastfeeding and the Baby Friendly
Hospital Initiative guidelines should become a minimum standard of care. Action is also
needed to improve the opportunities for women to breastfeed in public places and to
support continued breastfeeding in women who return to work.
The Healthy Start scheme provides support for eligible women and children through
provision of food vouchers and vitamin supplements, and needs to be promoted widely.
Its impact on the nutrition of mothers and young children should be evaluated at a
national level.
Other gaps in the evidence should be addressed including interventions to support

breastfeeding mothers in the workplace and interventions to optimise the timing and
content of complementary feeding.

Appendix 1: Epigenetic processes
In addition to the sequence of nucleotide bases which comprise the genetic code, and which are
inherited from the parents (the genotype) the characteristics of an individual (their phenotype) are
affected by epigenetic processes, which alter the ways in which genes are switched on and off.
Epigenetic processes do not affect the DNA sequence, but do alter gene expression. Epigenetic
changes occur during development and can be affected by the environment before and after birth.
Figure 15: Components of the epigenetic code
Me
The two main compoments

of the epigenetic code
Me DNA methylation
Me Methyl marks added to certain
DNA bases repress gene activity.
Me
Histone modification
A combination of different
molecules can attach to the tails
of proteins called histones. These
alter the activity of the DNA
Histone tails
wrapped around them.
Histones
Chromosomes
Diagram of chromosome being unravelled to show deoxyribonucleic acid (DNA) wrapped around histone protein
cores to form nucleosomes. Protruding histone tails are subject to a range of chemical modification which can
alter structure and make genomic DNA more accessible to transcription. CG base pairs of the DNA can also be
modified by methylation, which silences transcription. Thus these processes can affect gene expression, and
hence development and phenotypic characteristics, without altering the genomic DNA code itself.
Source: Qui J (2006) Epigenetics: unfinished symphony. Nature 441: 143-5.

Epigenetic inheritance is defined as biological processes that regulate mitotically or meiotically

284
heritable changes in gene expression without altering the DNA sequence. Of particular relevance
is methylation of specific CpG dinucleotides in gene promoters and alterations in DNA packaging
in nucleosomes arising from chemical modifications of the chromatin histone core around which
DNA wraps. The histone modifications include acetylation, methylation, ubiquitination, and
phosphorylation. Other changes may involve other DNA associated proteins. Recently microRNAs
which affect DNA transcription and mRNA stability and translation into proteins have been
285
implicated as a further mechanism for inherited epigenetic effects, including those transmitted
via the paternal line.
286
Epigenetic mechanisms are widely implicated in cancer. In this situation the changes can be
287
modified by alteration of methyl group metabolism. This suggests a mechanism by which folate
288
and methyl donor status during development may operate. Gene promoter methylation is
289 290, 291
important for asymmetrical silencing of imprinted genes and retrotransposons. They also
play a critical role in a range of developmental processes. With the exception of imprinted genes,
widespread removal of epigenetic marks occurs following fertilisation when maternal and paternal
genomes undergo extensive demethylation to ensure pluripotency of the developing embryonic
292, 293
cells. This is followed by de novo methylation just prior to implantation. About 70 per cent of
CpGs are methylated, mainly in repressive heterochromatin regions and in repetitive sequences
294
such as retrotransposable elements. DNA methylation also plays a key role in cell differentiation
by silencing the expression of specific genes during the development and differentiation of
individual tissues. For some genes there also appear to be gradations of promoter demethylation
associated with developmental changes in the role of the gene product. Changes in methylation
which are associated with cell differentiation and functional changes are established at different
times during development of the embryo. The pattern of DNA methylation is copied during mitosis
by DNA methyltransferase (Dnmt) -1 activity. This provides an epigenetic memory of patterns of
gene regulation and hence cell function, which are established during development and which are
292
passed to the adult. Environmental challenges at different times during development may induce
stable changes in cell function, which persist in the adult organism. They may produce different
phenotypic outcomes and in humans differential risk of disease.

Appendix 2: Definition of overweight
World Health Organisation classifications of BMI

BMI values are age-independent and the same for both sexes. It may not, however, correspond to
the same degree of fatness in different populations due, in part, to different body proportions. The
health risks associated with increasing BMI are continuous and the interpretation of BMI gradings
in relation to risk may differ for different populations.
Classification BMI (kg/m2)

Principal cut-off points Additional cut-off points
Underweight <18.50 <18.50

Severe thinness <16.00 <16.00
Moderate thinness 16.00 - 16.99 16.00 - 16.99
Mild thinness 17.00 - 18.49 17.00 - 18.49
Normal range 18.50 - 24.99 18.50 - 22.99

23.00 - 24.99
Overweight 25.00 25.00
Pre-obese 25.00 - 29.99 25.00 - 27.49
27.50 - 29.99
Obese 30.00 30.00
Obese class I 30.00 - 34-99 30.00 - 32.49
32.50 - 34.99
Obese class II 35.00 - 39.99 35.00 - 37.49
37.50 - 39.99
Obese class III 40.00 40.00
Source: World Health Organisation. Global Database on Body Mass Index: an interactive surveillance tool for
monitoring nutrition transition. www.who.int/bmi

Appendix 3: Current UK dietary

recommendations for pregnancy
Before pregnancy
A healthy diet is important at any time but particularly when planning a pregnancy. The Eatwell
249
plate makes healthy eating easier. Try to eat:
plenty of fruit and vegetables aim for at least five portions a day
plenty of starchy foods
some milk and dairy foods
some meat, fish, eggs and other non-dairy sources of protein
just a small amount of foods and drinks high in fat and/or sugar.
A 400g folic acid supplement should be taken daily from the time contraception is stopped until
the 12th week of pregnancy. Women who have previously had a baby with neural tube defects, or
who are taking medication for diabetes, epilepsy or coeliac disease should take a 5mg supplement.
DH guidelines on the consumption of alcohol state that women trying to conceive should avoid
drinking alcohol, but if they do choose to drink, to minimise the risk to the baby, they should not
drink more than one to two units of alcohol once or twice a week and should not get drunk.
During pregnancy
A healthy diet is important in pregnancy. There is no need to eat for two its the quality not the
quantity of the diet thats important. Try to eat a variety of foods including:
plenty of fruit and vegetables aim for at least five portions a day
plenty of starchy foods
plenty of iron-rich foods such as red meat, pulses, bread, green vegetables, and foods rich in
vitamin C that will help the iron to be absorbed
milk and dairy foods these contain calcium
foods rich in protein such as lean meat, chicken and fish (aim for at least two portions of fish
each week including one of oily fish), eggs and pulses
fibre-rich foods such as wholegrain bread and cereals.
Cut down on foods and drinks high in fat and/or sugar such as cakes and biscuits.
A 400g folic acid supplement should be taken daily until the 12th week of pregnancy. Women
who have previously had a baby with neural tube defects, or who are taking medication for
diabetes, epilepsy or coeliac disease should take a 5mg supplement.
A 10g vitamin D supplement should be taken throughout pregnancy.
Do not take dietary supplements that contain vitamin A such as fish liver oils, and avoid liver and
liver-containing products.
Caffeine-containing drinks should be consumed in moderation to limit caffeine intake to less than
200mg a day (equivalent to two mugs of instant coffee, two mugs of tea or five cans of cola).
Avoid pat, certain cheeses and raw or partially cooked eggs, shellfish and meats, and
unpasteurised milk.
DH guidelines on the consumption of alcohol state that pregnant women should avoid drinking alcohol
but if they do choose to drink, to minimise the risk to the baby they should not drink more than one to
two units of alcohol once or twice a week and should not get drunk. The BMA believe that the only
sensible message for women who are pregnant must be complete abstinence from alcohol.

www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_074920
www.eatwell.gov.uk/agesandstages/pregnancy/?lang=en
http://units.nhs.uk/pregnancy.html
Vegetarianism and veganism

It is possible for vegetarians and vegans (people who eat no animal products at all, including dairy
products) to be adequately nourished for successful pregnancy and lactation, but they need to be
knowledgeable about nutrition and plan their diet carefully. For vegans, there is a high risk of
deficient intakes of micronutrients such as vitamin B12, iodine, calcium, vitamin D and omega-3
fatty acids. There are reports of neurological deficits in children born to vitamin B12 deficient vegan
mothers. Vegan mothers should therefore take vitamin B12 supplements, as this micronutrient is
found only in foods of animal origin. The high levels of vitamin B12 found in some algae and
seaweeds (eg spirulina) are not bio-active. For the other micronutrients listed above, supplements
must be taken, or fortified foods (eg many soya milks are fortified with calcium) or specific foods
sources included in the diet (eg kelp seaweed for iodine, or flaxseed for omega-3 fatty acids).
295 296
Good advice can be found on the websites of the Vegetarian Society and Vegan Society.

Appendix 4: Infant feeding guidelines
159 118
World Health Organisation UK Food Standards Agency
Breastfeeding: Practice exclusive Breastfeeding: Breastfeeding is best and

breastfeeding from birth to six months, and provides all the nutrients a baby needs for
introduce complementary foods at six months the first six months. Continue exclusive
while continuing to breastfeed on-demand breastfeeding for six months. The longer
until two years of age or beyond. breastfeeding continues, the greater the
benefits.
Formula feeds: Not recommended all Formula feeds: Infant formula is the only
babies should be breastfed. WHO has alternative to breastfeeding until one year.
recently developed guidelines for the non- Cows milk-based formula is best. Follow-on
breastfed baby (partly for use by HIV-positive formula can be used from six months but is
297
women). not essential. Other types of formula should
be used only on medical advice: Hydrolysed
protein formula may be useful in cases of
cows milk allergy. Soya formula is an
alternative but may also be allergenic. Goats
milk formula is not suitable for babies.
Other drinks: Avoid giving drinks with low Other drinks: Water is the best alternative
nutrient value, such as tea, coffee and sugary drink to milk. Breastfed babies dont need
drinks such as soda. Limit the amount of juice any until they start solids. Under six months
offered so as to avoid displacing more use tap water, boiled and cooled. Some
nutrient-rich foods. Increase fluid intake bottled water has a mineral content too
during illness. high for babies. Others are suitable (labelled
accordingly). Bottled water should be boiled
too. Fruit juices are a source of vitamin C but
reduce the babys appetite for milk and can
cause tooth decay; avoid before six months.
After that use diluted (one in 10 with boiled
water) in a feeding cup, at mealtimes only.
Squashes, fizzy drinks, flavoured milk, juice
drinks, tea and coffee are not suitable for
infants.
Starting complementary feeds: Start at six Starting complementary feeds: Solids can
months with small amounts of food and be started from six months and gradually
increase as the child gets older while increased in amount and variety so that by
maintaining frequent breastfeeding. Energy twelve months, solid foods are the main part
needs from complementary foods in of the diet, with breast or formula milk
developing countries are ~200 kcal/day at making up the balance.
six to eight months, 300 kcal/day at nine to
11 months, and 550 kcal/day at 12-23
months. In industrialised countries these
estimates are 130, 310 and 580 kcal/day
because of differences in average breast
milk intake.

159 118
Progress with complementary feeds: Progress with complementary feeds: Start

Gradually increase food consistency and with a teaspoon of smooth vegetable pure
variety, adapting to the infants requirements (carrot, parsnip, potato, yam) or fruit pure
and abilities. Infants can eat pureed, mashed (banana, cooked apple, pear or mango) or
and semi-solid foods beginning at six months, cereal (not wheat-based) such as baby rice,
by eight months finger foods, by 12 months sago, maize, corn meal or millet, given with
the same types of food as the rest of the the babys usual milk (breast or formula) at
family, keeping in mind the need for nutrient- one feed in the day.
dense foods. Avoid foods that may cause
choking such as nuts, grapes, raw carrots. Gradually increase the amount within one
feed, and then progress to two and three
Increase the number of times the child is fed feeds per day. React to the babys appetite,
complementary foods as he/she gets older. giving more if wanted. Solids can include
For the average infant complementary foods full-fat cows milk products (yoghurt,
should be provided two to three times/day at fromage frais, cheese sauce). Give cereals
six to eight months and three to four once a day. Use home-cooked foods mashed,
times/day at nine to 24 months. Additional sieved, or pured. Introduce pured red meat,
nutritious snacks (pieces of fruit or bread or poultry, fish or eggs, or pured beans or
chapatti with nut paste) may be offered one pulses (lentils, hummus) at least once a day.
to two times/day. If the energy density or Serve starchy foods (potatoes, yams, rice or
amount of food per meal is low, or the child bread) two to three times/day, and fruit and
is no longer breastfed, more frequent meals vegetables as finger foods at two or more
may be required. meals/day.
Feed a variety of foods to ensure that As the baby continues to develop, use foods
nutrient needs are met. Meat, poultry, fish, with a thicker and lumpier texture to
eggs and vitamin A-rich foods should be encourage chewing, even before teeth
eaten daily or as often as possible. Provide emerge. Give finger foods (toast, bread,
diets with adequate fat content. After illness, breadsticks, pitta bread or chapatti, peeled
encourage the child to eat more than usual. apple, banana, carrot sticks, or cubes of
cheese). Avoid sweet biscuits and rusks. Later,
Vegetarian diets cannot meet nutrient needs start minced or chopped meals and fruit
at this age unless nutrient supplements or between meals. When the baby is mobile
fortified products are used. (crawling and walking) increase the amount
of food. Use full-fat dairy products; low fat is
sensible for adults but not babies.
If the family is vegetarian, use pulses (such as

red lentils, beans or chickpeas) or tofu as
protein sources. Vitamin C in fruit and
vegetables helps iron absorption, so include
these at mealtimes.

159 118
Do not force: Feed slowly and patiently; Do not force: Go at the babys pace. Allow
encourage but do not force. If children refuse plenty of time for feeding and to allow the
foods, experiment with different foods, tastes, baby to learn to swallow solids. Dont rush or
textures and methods of encouragement. force feed. Most babies know when theyve
Minimise distractions during meals. Feeding had enough to eat. Offer a wide variety of
times are periods of learning and love talk to foods to avoid choosiness later on.
children during feeding, with eye to eye contact.
Food safety: Practice good hygiene. Wash Food safety: Heat only what the baby will
hands before food preparation. Store foods want. Do not reheat previously warmed food.
safely. Serving immediately after preparation, Heat food thoroughly and allow it to cool.
using clean utensils and serving dishes. Avoid Do not refreeze food thats been warmed or
using feeding bottles, which are difficult to previously frozen. Everything for feeding the
keep clean. baby needs to be really clean.
To be avoided: No specific guidelines To be avoided: Added salt: Babies under a year

should have less than 1g salt per day. Dont add
salt to cooked foods. Limit high-salt foods
(cheese, bacon, sausages, processed foods, pasta
sauces, breakfast cereal).
Avoid sugar and honey: Sweeten stewed sour

fruit like rhubarb with mashed banana, breast or
formula milk. Dont use honey until after one
year as it may contain harmful bacteria. Some
foods can cause allergic reactions in some babies.
If a family history of coeliac disease, consult a

doctor before using wheat, rye or barley-based
foods. Nuts and seeds including peanuts,
peanut butter and other nut spreads. Dont give
whole peanuts to children under five years old
because they can cause choking.
Vitamin-mineral supplements: Use fortified Vitamin-mineral supplements: No specific

complementary foods or vitamin-mineral guidelines. See DH guidelines in text.
supplements as needed.
Starting ordinary cows milk: No specific Starting ordinary cows milk: Full-fat cows
guidelines. milk not suitable as a drink until one year.
Semi-skimmed milk not suitable as a drink
until two years. Skimmed milk not suitable
until five years.

Appendix 5: The International

Code on the Marketing of
Breast Milk Substitutes
The code was established by WHO in 1981 and has been modified by subsequent World Health
Assembly resolutions. The essential elements are as follows.
The Code forbids direct contacts between commercial representatives and medical personnel,
mothers or pregnant women.
Baby food companies may not distribute free or discounted samples of formula in hospitals and
other health premises.
Advertisements for baby foods must not target parents of infants younger than six months.
There should be no promotional distribution of dummies (pacifiers), bottles or teats.
Manufacturers of breast milk substitutes may not distribute promotional gifts to health workers,
and information produced for health professionals should be strictly factual and based on
scientific studies.
Images of mothers and children are not allowed on packaging. Information on labels must be
printed in easy to understand terms in the local language. Certain words, such as motherly,
cannot be used. The labels must state that breastfeeding is the best way of feeding babies and
that a substitute should only be used after consultation with health professionals.
The Code has no legal power unless it is incorporated into national legislatures (as in the UK).
Many developing countries have no effective legislation. The Code was initiated in response to
aggressive marketing of formula in developing countries in the 1970s and 80s. Code violations are
monitored by the International Baby Food Action Network (IBFAN) (www.ibfan.org); according to
IBFAN, violations are much less common but are still occurring.

Appendix 6: Comparison of the

nutrient composition of mature
human breast milk and formula
Mature Breast milk substitutes Follow-on
breast milk or first milks* Formula*
Energy (kcal) 670-700 670-700 670-700

(kJ) 2800-3000 2800-2950 2800-2950
Protein (g/l) 10-13 14-14.5 18-19
Casein (%) 35-40 40-43 78-80
-lactalbumin (%) 22-33 16 na
Lactoferrin (%) 10-15 0 0
Secretory IgA (%) 10-15 0 0
Lysozyme 1-4 0 0
Fat (g/l) 38-42 35-38 33-34
Saturated fat (%) 42 40-45 na
DHA (%) 0.07-1.0 0.2-0.5 varies
Carbohydrate (g/l) 69-74 70-75 74-81
Vitamins
A (g Re/l) 600 540-820 650-800
carotene (g Re/l) 24 35-42 25-43
* The composition of B1 (mg/l) 0.1-0.2 0.4-1.0 0.4-1.0
formula milk is presented B2 (mg/l) 0.3-0.4 0.6-1.5 1.0-1.5
as the range present in B3 (mg/l) 1.5-2.0 6.9-9.0 6.5-9.0
four leading brands B6 (mg/l) 0.1 0.4-0.6 0.4-0.6
each of cows milk-based B12 (g/l) 0.1-0.3 1.4-2.1 1.6-2.0
first and follow-on Folic acid (g/l) 50-52 34-160 70-150
preparations Biotin (g/l) 7.6 10-20 20-30
information supplied Pantothenic acid (mg/l) 2.0-2.6 2.3-3.0 3.0-3.6
by the manufacturers C (mg/l) 38-43 69-90 80-140
(date 31 January 2008). D (g/l) 0.1-0.4 10-14 11-19
Breast milk varies in E (mg/l) 2.0-3.5 5-13 5-11
composition and K (g/l) 15 27-67 29-67
therefore the values Minerals and trace elements
provided are approximate; Sodium (mg/l) 150-160 160-170 200-300
information on the Potassium (mg/l) 550-600 570-740 850-900
composition of breast Calcium (mg/l) 300-360 390-510 720-900
milk was obtained from Phosphorus (mg/l) 140-155 240-290 480-530
126, 127, 298-301
several sources. Ca/P ratio 1.7-1.8 1.4-2.0 1.2-1.7
Iron (mg/l) 0.5-0.8 5-8 12-3
na in the table indicates Zinc (mg/l) 3-4 3-6 4-9
that the authors of this Iodine (g/l) 30-70 45-100 100-120
study were unable to Copper (g/l) 384-400 330-420 410-600
find the relevant data. Selenium (g/l) 10-30 10-15 15
Magnesium (mg/l) 29-40 45-52 65-70
Source: Hamosh 2001, Other
Prentice 1996, Williams Cholesterol (mmol/l) 163 0 0
1998, Behrman 1987, Taurine (mg/l) 40-54 47-67 50
Golden 2000.


References
1. Gluckman PD & Hanson MA (eds) (2006) Developmental origins of health and disease.
Cambridge: Cambridge University Press.
2. Henderson L, Gregory J & Swan G (2002) The national diet & nutrition survey: adults aged
19 to 64 years. Volume 1. London: The Stationery Office.
3. Black RE, Allen LH, Bhutta ZA et al (2008) Maternal and child undernutrition: global and
regional exposures and health consequences. Lancet 371: 243-60.
4. International Obesity Task Force. The global epidemic. www.iotf.org/intro/global.htm
5. Cordain L, Eaton SB, Sebastian A et al (2005) Origins and evolution of the Western diet:
health implications for the 21st century. American Journal of Clinical Nutrition 81: 341-54.
6. Jackson AA (1991) The glycine story. European Journal of Clinical Nutrition 45: 59-65.
7. Jackson AA (1996) Perinatal nutrition: the impact on postnatal growth and development.
In: Gluckman PD & Heymann MA (eds) Pediatrics and perinatalogy: the scientific basis.
London: Arnold.
8. Kramer MS & Kakuma R (2003) Energy and protein intake in pregnancy. Cochrane
Database of Systematic Reviews CD000032.
9. Haider BA & Bhutta ZA (2006) Multiple-micronutrient supplementation for women during
pregnancy. Cochrane Database of Systematic Reviews CD004905.
10. Barker DJP (1998) Mothers, babies and health in later life. London: Churchill Livingstone.
11. Hales CN & Barker DJP (2001) The thrifty phenotype hypothesis. British Medical Bulletin
60: 5-20.
12. Gluckman PD & Hanson MA (2004) Living with the past: evolution, development, and
patterns of disease. Science 305: 1733-6.
13. Gluckman PD & Hanson MA (2006) Mismatch why our world no longer fits our bodies.
Oxford: Oxford University Press.
14. Department of Health (2006) Forecasting obesity to 2010. London: Department of Health.
15. Scottish Executive (2005) The Scottish health survey 2003. Edinburgh: Scottish Executive.
16. Office for National Statistics (2007) Welsh health survey 2005/06. Cardiff: Welsh Assembly
Government.
17. Northern Ireland Statistics and Research Agency (2007) Northern Ireland health and social
wellbeing survey 2005/06. Belfast: Northern Ireland Statistics and Research Agency.
18. Government Office for Science (2007) Tackling obesity: future choices summary of key
messages. London: Department for Innovation, Universities and Skills.
19. Victora CG, Adair L, Fall C et al (2008) Maternal and child undernutrition: consequences for
adult health and human capital. Lancet 371: 340-57.
20. Wild S, Roglic G, Green A et al (2004) Global prevalence of diabetes; estimates for the year
2000 and projections for 2030. Diabetes Care 27: 1047-53.
21. World Health Organisation (2005) Cardiovascular disease prevention and control:
translating evidence into action. Geneva: World Health Organisation.
22. Rogers I (2005) Birth weight and obesity and fat distribution in later life; a review. Birth
Defects Research Part A: Clinical and Molecular Teratology 73: 485-6.
23. Yajnik CS, Fall CHD, Coyaji KJ et al (2003) Neonatal anthropometry: the thin-fat Indian
baby; the Pune Maternal Nutrition Study. International Journal of Obesity 27: 173-80.
24. Vickers MH, Breier BH & Cutfield WS (2000) Fetal origins of hyperphagia, obesity, and
hypertension and postnatal amplification by hypercaloric nutrition. American Journal of
Physiology Endocrinology and Metabolism 279: E83-7.
25. Jackson AA & Wootton SA (1989) The energy requirements of growth and catch-up
growth. In: Schurch B & Scrimshaw NS (eds) Activity, energy expenditure and energy
requirements of infants and children international dietary energy consultancy group.
Cambridge, Massachusetts: International Dietary Energy Consultancy Group.

26. Boney CM, Verma A, Tucker R et al (2005) Metabolic syndrome in childhood: association
with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics 115:
e290-6.
27. Hillier TA, Mullen JA & Pedula KL (2007) Childhood obesity and metabolic imprinting.
The ongoing effects of maternal hyperglycemia. Diabetes Care 30: 2287-92.
28. Williams MA, Emanuel I, Kimpo C et al (1999) A population-based cohort study of the
relation between maternal birthweight and risk of gestational diabetes mellitus in four
racial/ethnic groups. Paediatric and Perinatal Epidemiology 14: 378-80.
29. British Medical Association (1999) Growing up in Britain: ensuring a healthy future for our
children. London: British Medical Association.
30. Hoet JJ & Hanson MA (1999) Intrauterine nutrition: its importance during critical periods for
cardiovascular and endocrine development. Journal of Physiology 514: 617-27.
31. Myatt L & Roberts V (2006) Placental mechanisms and developmental origins of health and
disease. In: Gluckman PD & Hanson MA (eds) Developmental origins of health and disease.
Cambridge: Cambridge University Press.
32. Drner G (1973) Possible significance of prenatal and-or perinatal nutrition for the
pathogenesis of obesity. Acta Biologica et Medica Germanica 30: K19-22.
33. Drner G, Haller H & Leonhardt W (1973) Possible significance of pre- and/or early
postnatal nutrition in the pathogenesis of arteriosclerosis. Acta Biologica et Medica
Germanica 31: K31-5.
34. Drner G & Mohnike A (1973) Possible significance of pre- and/or early postnatal nutrition
in the pathogenesis of diabetes mellitus. Acta Biologica et Medica Germanica 31: K7-10.
35. Drner G, Plagemann A & Reinagel H (1987) Familial diabetes aggregation in type 1
diabetics: gestational diabetes an apparent risk factor for increased diabetes susceptibility in
the offspring. Experimental and Clinical Endocrinology 89: 84-90.
36. Gennser G, Rymark P & Isberg PE (1988) Low birth weight and risk of high blood pressure
in adulthood. British Medical Journal 28: 1498-500.
37. Forsdahl A (1978) Living conditions in childhood and subsequent development of risk
factors for arteriosclerotic heart disease. The cardiovascular survey in Finnmark 1974-75.
Journal of Epidemiology and Community Health 32: 34-7.
38. Singhal A & Lucas A (2004) Early origins of cardiovascular disease: is there a unifying
hypothesis? Lancet 363: 1642-5.
39. Barker DJ & Osmond C (1986) Infant mortality, childhood nutrition and ischaemic heart
disease in England and Wales. Lancet 1: 1077-81.
40. Huxley R, Owen CG, Whincup PH et al (2007) Is birth weight a risk factor for ischemic heart
disease in later life? American Journal of Clinical Nutrition 85: 1244-50.
41. Jacob F & Monod J (1961) Genetic regulatory mechanisms in the synthesis of proteins.
Journal of Molecular Biology 3: 318-56.
42. Nowacki M, Vijayan V, Zhou Y et al (2008) RNA-mediated epigenetic programming of a
genome-rearrangement pathway. Nature 451: 153-8.
43. Huxley R, Neil A & Collins R (2002) Unravelling the fetal origins hypothesis: is there really
an inverse association between birth weight and subsequent blood pressure? Lancet 360:
659-65.
44. Curhan GC, Chertow GM, Willett WC et al (1996) Birth weight and adult hypertension and
obesity in women. Circulation 94: 1310-5.
45. Whincup PH, Cook DG, Adshead F et al (1997) Childhood size is more strongly related than
size at birth to glucose and insulin levels in 10-11-year-old children. Diabetologia 40: 319-26.
46. Lucas A, Fewtrell MS & Cole TJ (1999) Fetal origins of adult disease the hypothesis
revisited. British Medical Journal 319: 245-9.

47. Osmond C, Barker DJP, Winter PD et al (1993) Early growth and death from cardiovascular
disease in women. British Medical Journal 307: 1519-24.
48. Barker DJP, Osmond C, Forsen TJ et al (2005) Trajectories of growth among children who
have coronary events as adults. New England Journal of Medicine 353: 1802-9.
49. Eriksson JG, Forsen T, Tuomilehto HJ et al (2001) Early growth and coronary heart disease in
later life: longitudinal study. British Medical Journal 322: 949-53.
50. Gluckman PD, Hanson MA, Spencer HG et al (2005) Environmental influences during
development and their later consequences for health and disease: implications for the
interpretation of empirical studies. Proceedings of the Royal Society 272: 671-7.
51. Koupilova I, Leon DA, McKeigue PM et al (1999) Is the effect of birth weight on
cardiovascular mortality mediated through high blood pressure? Journal of Hypertension
17: 19-25.
52. Rich-Edwards J, Stampfer MJ, Manson JE et al (1997) Birth weight and risk of cardiovascular
disease in a cohort of women followed up since 1976. British Medical Journal 315: 396-400.
53. Kajantie E, Osmond C, Barker D et al (2005) Size at birth as a predictor of mortality in
adulthood: a follow-up study of 350,000 person-years. International Journal of
Epidemiology 34: 655-63.
54. Lawlor DA, Ronalds G & Clark H (2005) Birth weight is inversely associated with incident
coronary heart disease and stroke among individuals born in the 1950s: findings from the
Aberdeen Children of the 1950s prospective cohort study. Circulation 112: 1414-8.
55. Bergvall N, Iliadou A, Tuvemo T et al (2005) Birth characteristics and risk of high systolic
blood pressure in early adulthood: socio-economic factors and familial effects. Epidemiology
16: 635-40.
56. Vasan RS, Pencine MJ, Cobain M et al (2005) Estimated risks for developing obesity in the
Framingham Study. Annals of Internal Medicine 143: 473-80.
57. Gamborg M, Byberg L, Rasmussen F et al (2007) Birth weight and systolic blood pressure in
adolescence and adulthood: meta-regression and analysis of sex- and age-specific results
from 20 Nordic studies. American Journal of Epidemiology 166: 634-45.
58. Hardy R, Wadsworth ME, Langenberg C et al (2004) Birth weight, childhood growth and
blood pressure at 43 years in a British birth cohort. International Journal of Epidemiology
33: 121-9.
59. Newsome CA, Shiell AW, Fall CHD et al (2003) Is birth weight related to later glucose and
insulin metabolism? A systematic review. Diabetic Medicine 20: 339-48.
60. Kensara OA, Wootton SA, Phillips DI et al (2005) Fetal programming of body composition:
relation between birth weight and body composition measured with dual-energy x-ray
absorptiometry and anthropometric methods in older Englishmen. American Journal of
Clinical Nutrition 82: 980-7.
61. Bertram CE & Hanson MA (2001) Animal models and programming of the metabolic
syndrome. British Medical Bulletin 60: 103-21.
62. McMillen IC & Robinson JS (2005) Developmental origins of the metabolic syndrome:
prediction, plasticity, and programming. Physiological Reviews 85: 571-633.
63. Armitage J, Taylor P & Poston L (2005) Experimental models of developmental
programming; consequences of exposure to an energy rich diet during development.
Journal of Physiology 565: 3-8.
64. Bayol SA, Farrington SJ & Stickland NC (2007) A maternal junk food diet in pregnancy and
lactation promotes an exacerbated taste for junk food and a greater propensity for obesity
in rat offspring. British Journal of Nutrition 98: 843-51.
65. Samuelsson A-M, Matthews PA, Argenton M et al (2008) Diet induced obesity in female
mice leads to offspring hyperphagia, adiposity, hypertension and insulin resistance: a novel
murine model of developmental programming. Hypertension 51: 383-92.

66. Vickers MH (2007) Developmental programming and adult obesity: the role of leptin.
Current Opinion in Endocrinology, Diabetes and Obesity 14: 17-22.
67. Vickers MH, Breier BH, McCarthy D et al (2003) Sedentary behaviour during postnatal life is
determined by the prenatal environment and exacerbated by postnatal hypercaloric
nutrition. American Journal of Physiology 285: R271-3.
68. Jackson AA, Dunn RL, Marchand MC et al (2002) Increased systolic blood pressure in rats
induced by a maternal low-protein diet is reversed by dietary supplementation with glycine.
Clinical Science 103: 633-9.
69. Brawley L, Torrens C, Anthony FW et al (2004) Glycine rectifies vascular dysfunction induced
by dietary protein imbalance during pregnancy. Journal of Physiology 554: 497-504.
70. Torrens C, Brawley L, Anthony FW et al (2006) Folate supplementation during pregnancy
improves offspring cardiovascular dysfunction induced by protein restriction. Hypertension
47: 982-7.
71. Vickers MH, Gluckman PD, Coveny AH et al (2005) Neonatal leptin treatment reverses
developmental programming. Endocrinology 146: 4211-6.
72. Elahi MM, Cagampang FR, Anthony FW et al (2008) Statin treatment in
hypercholesterolemic pregnant mice reduces cardiovascular risk factors in their offspring.
Hypertension 51: 1-2.
73. Burdge GC, Slater-Jefferies J, Torrens C et al (2007) Dietary protein restriction of pregnant
rats in the F0 generation induces altered methylation of hepatic gene promoters in the
adult male offspring in the F1 and F2 generations. British Journal of Nutrition 97: 435-9.
74. Torrens C, Anthony FW, Poston L et al (2008). Transmission of raised blood pressure and
endothelial dysfunction induced to the F2 generation induced by maternal protein
restriction in the F0, in the absence of dietary challenge in the F1 generation. British Journal
of Nutrition 100: 760-6.
75. Gluckman PD, Hanson MA & Beedle AS (2007) Non-genomic transgenerational inheritance
of disease risk. BioEssays 29: 145-54.
76. Kwong WY, Wild AE, Roberts P et al (2000) Maternal undernutrition during the
preimplantation period of rat development causes blastocyst abnormalities and
programming of postnatal hypertension. Development 127: 4195-202.
77. Watkins AJ, Ursell E & Panton R (2008) Adaptive responses by mouse early embryos to
maternal diet protect fetal growth and predispose to adult onset disease. Biology of
Reproduction 87: 299-306.
78. Edwards LJ & McMillen IC (2002) Periconceptional nutrition programs development of the
cardiovascular system in the fetal sheep. American Journal of Physiology Regulatory,
Integrative and Comparative Physiology 283: R669-79.
79. Gardner DS, Van Bon BWM, Dandrea J et al (2006) Effect of periconceptional
undernutrition and gender on hypothalamic-pituitary-adrenal axis function in young adult
sheep. Journal of Endocrinology 190: 203-12.
80. Cleal JK, Poore KR, Boullin JP et al (2007) Mismatched pre- and postnatal nutrition leads to
cardiovascular dysfunction and altered renal function in adulthood. Proceedings of the
National Academy of Sciences 104: 9529-33.
81. Rumball CWH, Harding JE, Oliver MH et al (2008) Effects of twin pregnancy and
periconceptional undernutrition on maternal metabolism, fetal growth and glucose-insulin
axis function in ovine pregnancy. Journal of Physiology 586: 1399-411.
82. Poore KR, Cleal JK, Newman JP et al (2007) Nutritional challenges during development
induce sex-specific changes in glucose homeostasis in the adult sheep. American Journal of
Physiology Endocrinology and Metabolism 292: E32-9.

83. Watkins AJ, Platt D, Papenbrock T et al (2007) Mouse embryo culture induces changes in
postnatal phenotype including raised systolic blood pressure. Proceedings of the National
Academy of Sciences of the United States of America 104: 5449-54.
84. Van Speybroeck L (2002) From epigenesis to epigenetics. The case of CH Waddington.
Annals of the New York Academy of Sciences 981: 61-81.
85. Schmalhausen IL (1949) Factors of evolution. New York: Blakiston (McGraw-Hill).
86. Leary SD, Smith GD, Rogers IS et al (2006) Smoking during pregnancy and offspring fat and
lean mass in childhood. Obesity 14: 2284-93.
87. Martin RM, Smith GD, Frankel S et al (2004) Parents growth in childhood and the birth
weight of their offspring. Epidemiology 15: 308-16.
88. Barker DJP (1995) The fetal origins of coronary heart disease. British Medical Journal
311: 171-4.
89. Adair LS, Kuzawa BBA & Borja J (2001) Maternal energy stores and diet composition during
pregnancy program adolescent blood pressure. Circulation 104: 1034-9.
90. Godfrey KM, Forrester T, Barker DJP et al (1994) Maternal nutritional status in pregnancy and
blood pressure in childhood. British Journal of Obstetrics and Gynaecology 101: 398-403.
91. Jie M, Law C, Zhang K-L et al (2000) Effects of infant birth weight and maternal body mass
index in pregnancy on components of the Insulin Resistance Syndrome in China. Annals of
Internal Medicine 132: 253-60.
92. Erikksson JG, Forsen T, Tuomilhehto J et al (2002) Effects of size at birth and childhood
growth on the insulin resistance syndrome in elderly individuals. Diabetologia 45: 342-8.
93. Stein C, Fall CHD, Kumaran K et al (1996) Fetal growth and coronary heart disease in South
India. Lancet 348: 1269-73.
94. Roseboom TJ, van der Meulen J, Ravelli ACJ et al (2001) Effects of prenatal exposure to the
Dutch famine on adult disease in later life: an overview. Molecular and Cellular
Endocrinology 185: 93-8.
95. Stein AD, Wang M & Ramirez-Zea M (2006) Exposure to a nutrition supplementation
intervention in early childhood and risk factors for cardiovascular disease in adulthood:
evidence from Guatemala. American Journal of Epidemiology 164: 1160-70.
96. Drner G & Plagemann A (1994) Perinatal hyperinsulinism as possible predisposing factor
for diabetes mellitus, obesity and enhanced cardiovascular risk in later life. Hormonal and
Metabolic Research 26: 213-21.
97. Yajnik CS, Deshpande SS, Jackson AA et al (2008) Vitamin B12 and folate concentrations
during pregnancy and insulin resistance in the offspring: the Pune Maternal Nutrition Study.
Diabetologia 51: 29-38.
98. Gluckman PD, Yap Seng C, Fukuoka H et al (2007) Low birthweight and subsequent
obesity in Japan. Lancet 369: 1081-2.
99. Catalano P (2003) Obesity and pregnancy the propagation of a vicious cycle? Journal of
Clinical Endocrinology and Metabolism 88: 3505-6.
100. Oken E & Gillman MW (2003) Fetal origins of obesity. Obesity Research 11: 496-506.
101. Rich-Edward JW, Colditz GA, Stampfer MJ et al (1999) Birthweight and the risk of type 2
diabetes in adult women. Annals of Internal Medicine 130: 278-84.
102. Wei J-N, Sung F-C, Li C-Y et al (2003) Low birth weight and high birth weight infants
are both at an increased risk to have type 2 diabetes among schoolchildren in Taiwan.
Diabetes Care 26: 343-8.
103. Krishnaveni GV, Hill JC, Leary S et al (2005) Anthropometry, glucose tolerance and insulin
concentrations in Indian children: relationships to maternal glucose and insulin
concentrations during pregnancy. Diabetes Care 28: 2919-25.
104. Dabelea D, Hanson RL, Lindsay RS et al (2000) Intrauterine exposure to diabetes conveys
risks for type 2 diabetes and obesity. A study of discordant sibships. Diabetes 49: 2208-11.

105. Dabelea D & Pettitt DJ (2001) Intrauterine diabetic environment confers risks for type 2
diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. Journal of
Pediatric Endocrinology and Metabolism 14: 1085-91.
106. Catalano PM, Thomas A, Huston-Presley L et al (2003) Increased fetal adiposity: a very
sensitive marker of abnormal in utero development. American Journal of Obstetrics and
Gynaecology 189: 1698-704.
107. Moses RG, Luebcke M, Davis WS et al (2006) Effect of a low-glycemic-index diet during
pregnancy on obstetric outcomes. American Journal of Clinical Nutrition 84: 807-12.
108. Singhal A, Wells J, Cole TJ et al (2003) Programming of lean body mass: a link between
birth weight, obesity and cardiovascular disease? American Journal of Clinical Nutrition
77: 726-30.
109. Sayer AA, Syddall HE & Dennison EM (2004) Birth weight, weight at 1 y of age, and body
composition in older men: findings from the Hertfordshire Cohort Study. American Journal
of Clinical Nutrition 80: 199-203.
110. Sewell MF, Huston-Presley L & Super DM (2006) Increased neonatal fat mass, not lean body
mass, is associated with maternal obesity. American Journal of Obstetrics and Gynecology
195: 110-3.
111. Ness AR (2004) The Avon Longitudinal Study of Parents and Children (ALSPAC) a resource
for the study of the environmental determinants of childhood obesity. European Journal of
Endocrinology 151: U141-9.
112. Inskip H, Godfrey KM, Robinson SM et al (2006) Cohort profile: the Southampton Womens
Survey. International Journal of Epidemiology 35: 42-8.
113. Haugen G, Hanson M, Kieerud T et al (2005) Fetal liver-sparing cardiovascular adaptations
linked to mothers slimness and diet. Circulation Research 96: 12-4.
114. Drake AJ, Walker BR & Seckle JR (2005) Intergenerational consequences of fetal
programming by in utero exposure to flucocorticoids in rats. American Journal of Physiology
Regulatory, Integrative and Comparative Physiology 288: R34-8.
115. Kaati G, Bygren LO, Pembrey M et al (2007) Transgenerational response to nutrition, early
life circumstances and longevity. European Journal of Human Genetics 15: 784-90.
116. Department of Health (1999) Dietary reference values for food energy and nutrients for the
United Kingdom: report of the Panel on Dietary Reference Values of the Committee on
Medical Aspects of Food Policy. London: The Stationery Office.
117. Department of Health (1994) Weaning and the weaning diet: report of the Working Group
on the Weaning Diet of the Committee on Medical Aspects of Food Policy. London: The
Stationery Office.
118. Food Standards Agency. Weaning your baby.
www.eatwell.gov.uk/agesandstages/baby/weaning
119. Office for National Statistics (2007) Health statistics quarterly 35: infant and perinatal
mortality 2006: health areas, England and Wales. London: Office for National Statistics.
120. Ananth CV & Platt RW (2004) Reexamining the effects of gestational age, fetal growth and
maternal smoking on neonatal mortality. BioMed Central Pregnancy and Childbirth 4: 22.
121. Maher J & Macfarlane A (2004) Inequalities in infant mortality: trends by social class,
registration status, mothers age and birth weight, England and Wales, 1976. Health
Statistics Quarterly 24: 14-22.
122. Shrimpton R, Victora CG, de Onis M et al (2001) Worldwide timing of growth faltering;
implications for nutritional interventions. Pediatrics 107: E75.
123. Bhutta ZA, Ahmed T, Black RE et al (2008) What works? Interventions for maternal and
child undernutritrion and survival. Lancet 371: 417-40.
124. The World Bank (2006) Repositioning nutrition as central to development; a strategy for
large-scale action. Washington DC: The World Bank.

125. Hoddinot J, Maluccio JA, Behrman JR et al (2008) Effect of a nutrition intervention during
early childhood on economic productivity in Guatemala adults. Lancet 371: 411-6.
126. Prentice A (1996) Constituents of human milk. Food and Nutrition Bulletin 17.
127. Hamosh M (2001) Bioactive factors in human milk. Pediatric Clinics of North America
48: 69-86.
128. ODowd R, Kent JC, Moseley JM et al (2007) The effects of uteroplacental insufficiency and
reduced litter size on mammary function and postnatal offspring growth. American Journal
of Physiology Regulatory, Integrative and Comparative Physiology 294: R539-48.
129. Pico C, Oliver P, Sanchez J et al (2007) The intake of physiological doses of leptin during
lactation in rats prevents obesity in later life. International Journal of Obesity 31: 1199-209.
130. Armstrong J & Reilly JJ (2002) Breastfeeding and lowering the risk of childhood obesity.
Lancet 359: 2003-4.
131. Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The
Information Centre.
132. Lande B, Anderson LF, Baerug A et al (2003) Infant feeding practices and associated factors
in the first six months of life: the Norwegian Infant Nutrition Survey. Acta Paediatrica
92: 152-61.
133. Wright CM, Parkinson K & Scott J (2006) Breastfeeding in a UK urban context: who
breastfeeds, for how long and does it matter? Public Health Nutrition 9: 686-91.
134. McFadden A & Toole G (2006) Exploring womens views of breastfeeding: a focus group
study within an area with high levels of socio-economic deprivation. Maternal and Child
Nutrition 2: 156-68.
135. Cowin I & Emmett P (2000) Diet in a group of 18-month-old children in South West
England, and comparison with the results of a national survey. Journal of Human Nutrition
& Dietetics 13: 87-100.
136. Noble S, Emmett P and the ALSPAC team (2001) Food and nutrient intakes in a cohort of
8-month old infants in the South West of England in 1993. European Journal of Clinical
137. Northstone K, Rogers I, Emmett P et al (2002) Drinks consumed by 18-month-old children:
are current recommendations being followed? European Journal of Clinical Nutrition
56: 236-44.
138. Robinson S, Marriott L, Poole J et al (2007) Dietary patterns in infancy: the importance of
maternal and family influences on feeding practice. British Journal of Nutrition 98: 1029-37.
139. Robinson S, Crozier SR, Borland SE et al (2004) Impact of educational attainment on the
quality of young womens diets. European Journal of Clinical Nutrition 58: 1174-80.
140. Oliveria SA, Ellison RC, Moore LL et al (1992) Parent-child relationships in nutrient intake:
the Framingham Childrens Study. American Journal of Clinical Nutrition 56: 593-8.
141. Birch LL & Fisher JO (1998) Development of eating behaviors among children and
adolescents. Pediatrics 101: 539-49.
142. Vereecken CA, Keukelier E & Maes L (2004) Influence of mothers educational level on food
parenting practices and food habits of young children. Appetite 43: 93-103.
143. Fewtrell MS, Morgan JB, Duggan C et al (2007) Optimal duration of exclusive
breastfeeding: what is the evidence to support current recommendations. American Journal
of Clinical Nutrition 85: 635S-8S.
144. Reilly JJ & Wells JCK (2005) Duration of breast-feeding: introduction of complementary
feeding may be necessary before 6 months of age. British Journal of Nutrition 94: 869-72.
145. Raiten DJ, Kalhan SC & Hay WW (2007) Maternal nutrition and optimal infant feeding
practices: executive summary. American Journal of Clinical Nutrition 85: 577S-83S.
146. Kramer M & Kakuma R (2004) The optimal duration of breast feeding; a systematic review.
Advances in Experimental Biology 554: 63-77.

147. Collaborative Group on Hormonal Factors in Breast Cancer (2002) Breast cancer and
breastfeeding: collaborative reanalysis of individual data from 47 epidemiological studies in
30 countries, including 50,302 women with breast cancer and 96,973 women without the
disease. Lancet 360: 187-95.
148. Department of Health (2004) Good practice and innovation in breastfeeding. London:
Department of Health.
149. National Institute for Health and Clinical Excellence (2008) Improving the nutrition of
pregnant and breastfeeding women and children in low income households: NICE Public
Health Guidance 11.
150. Food Standards Agency. Breastfeeding your baby.
www.eatwell.gov/agesandstages/baby/breastfeed
151. Allen L (2005) Multiple micronutrients in pregnancy and lactation; an overview. American
Journal of Clinical Nutrition 81: 1206S-12S.
152. British Medical Association and Royal Pharmaceutical Society of Great Britain (2008) British
National Formulary 2008. London: British Medical Association and Royal Pharmaceutical
Society of Great Britain.
153. Ilett KF & Kristensen JH (2005) Drug use and breastfeeding. Expert Opinion 4: 745-68.
154. Anderson PO, Pochop SL & Manoquerra AS (2003) Adverse drug reactions in breast fed
infants; less than imagined. Clinical Pediatrics 42: 325-40.
155. HM Government (1995) The infant formula and follow-on formula regulations 1995.
London: The Stationery Office.
156. Koletzko B, Aggett PJ, Bindels JG et al (1998) Growth, development and differentiation: a
functional food science approach. British Journal of Nutrition 80: S5-S45.
157. Koletzko B, Lien E, Agostini C et al (2008) The roles of long-chain polyunsaturated fatty
acids in pregnancy, lactation and infancy: a review of current knowledge and consensus
recommendations. Journal of Perinatal Medicine 36: 5-14.
158. Royal College of Paediatrics and Child Health (1999) Medicines for children. London: Royal
College of Paediatrics and Child Health.
159. Daelmans B, Martines J, & Saadeh R (eds) (2003) Special issue based on a World Health
Organization expert consultation on complementary feeding. Food and Nutrition Bulletin
24: 1-134.
160. Ong KK, Preece MA, Emmett PM et al (2002) Size at birth and early childhood growth in
relation to maternal smoking, parity and infant breastfeeding: longitudinal birth cohort
study and analysis. Pediatric Research 52: 863-7.
161. Kramer M, Guo T, Platt RW et al (2004) Feeding effects on growth in infancy. Journal of
Pediatrics 145: 600-5.
162. Dewey KG, Heinig MJ, Nommsen LA et al (1992) Growth of breastfed and formula-fed
infants from 0 to 18 months: the DARLING study. Pediatrics 89: 1035-41.
163. Fewtrell MS, Morley R & Abbott RA (2001) Catch up growth in small-for-gestational-age
term infants: a randomised trial. American Journal of Clinical Nutrition 74: 516-23.
164. Karlberg J, Engstrom I, Karleberg P et al (1987) Analysis of linear growth using a
mathematical model. I. From birth to three years. Acta Paediatrica Scandinavica 76: 478-88.
165. Law C (2005) Early growth and chronic disease: a public health overview. Maternal and
Child Nutrition 1: 169-76.
166. Lucas P, Arai L, Baird J et al (2007) A systematic review of lay views on infant size and
growth. Archives of Disease in Childhood 92: 120-7.
167. Freeman JV, Cole TJ, Chinn S et al (1995) Cross sectional stature and weight reference
curves for the UK, 1990. Archives of Disease in Childhood 73: 17-24.
168. Cole TJ, Freeman JV & Preece MA (1995) Body mass index reference curves for the UK,
1990. Archives of Disease in Childhood 73: 25-9.

169. www.childgrowthfoundation.org
170. World Health Organisation (2006) WHO child growth standards: length/height-for-age,
weight-for-age, weight-for-length, weight-for-height and body mass index-for-age. Geneva:
World Health Organisation.
171. Dewey KG, Peerson JM, Brown KH et al (1995) Growth of breastfed infants deviates from
current reference data: a pooled analysis of US, Canadian and European datasets. Pediatrics
96: 495-503.
172. Scientific Advisory Committee on Nutrition & Royal College of Paediatrics and Child Health
(2007) Application of WHO growth standards in the UK. London: The Stationery Office.
173. Howie PW, Forsyth JS, Ogston SA et al (1990) Protective effect of breastfeeding against
infection. British Medical Journal 300: 11-6.
174. Cunningham AS, Jelliffe DB & Jelliffe EFP (1991) Breastfeeding and health in the 1980s: a
global epidemiologic review. Journal of Pediatrics 118: 659-66.
175. Forsyth JS (1995) The relationship between breastfeeding and infant health and
development. Proceedings of the Nutrition Society 54: 407-18.
176. American Academy of Pediatrics (1997) Breastfeeding and the use of human milk.
Pediatrics 100: 1035-9.
177. Dyson L, Renfrew M, McFadden A et al (2006) Promotion of breastfeeding initiation and
duration; evidence into practice briefing. London: National Institute for Health and Clinical
Excellence.
178. McCance RA (1962) Food, growth and time. Lancet II: 621-6.
179. Ashwell M (1993) McCance and Widdowson; a scientific partnership of 60 years. London:
British Nutrition Foundation.
180. Kramer MS, Matush L, Vanilovich I et al (2007) Effects of prolonged and exclusive
breastfeeding on child height, weight, adiposity, and blood pressure at age 6.5 years:
evidence from a large randomised trial. American Journal of Clinical Nutrition 86: 1717-21.
181. Koletzko B (2006) Long-term consequences of early feeding on later obesity risk. Nestl
Nutrition Workshop Series: Pediatric Program 58: 1-18.
182. Villalpando S & Hamosh M (1998) Early and late effects of breastfeeding: does
breastfeeding really matter? Biology of the Neonate 74: 177-91.
183. Reynolds A (2001) Breastfeeding and brain development. Pediatric Clinics of North America
48: 159-71.
184. Jain A, Concato J & Leventhal JM (2002) How good is the evidence linking breastfeeding
and intelligence? Pediatrics 109: 1044-53.
185. Der G, Batty GD & Deary IJ (2006) Effect of breastfeeding on intelligence in children;
prospective study, sibling pairs analysis and meta-analysis. British Medical Journal 333: 929-30.
186. Lucas A, Morley R & Isaacs E (2001) Nutrition and mental development. Nutrition Reviews
59: S24-33.
187. Arenz S, Ruckerl R, Koletzko B et al (2004) Breastfeeding and childhood obesity a
systematic review. International Journal of Obesity and Related Metabolic Disorders 28:
1247-56.
188. Owen CG, Martin RM, Whincup PH et al (2005) Effect of infant feeding on the risk of
obesity across the life course: a quantitative review of published evidence. Pediatrics 115:
1367-77.
189. Owen CG, Martin RM, Whincup PH et al (2005) The effect of breastfeeding on mean body
mass index throughout life: a quantitative review of published and unpublished
observational evidence. American Journal of Clinical Nutrition 82: 1298-1307.
190. Harder T, Bergmann R, Kallischnigg G et al (2005) Duration of breastfeeding and risk of
overweight: a meta-analysis. American Journal of Epidemiology 162: 397-403.

191. Baker JL, Michaelsen KF, Sorensen TI et al (2007) High prepregnant body mass index is
associated with early termination of full and any breastfeeding in Danish women. American
Journal of Clinical Nutrition 86: 404-11.
192. Toschke AM, Martin RM, von Kries R et al (2007) Infant feeding method and obesity: body
mass index and dual X-ray absorptiometry measurements at 9-10 y of age from the Avon
Longitudinal Study of Parents and Children (ALSPAC). American Journal of Clinical Nutrition
85: 1578-85.
193. Rolland-Cachera MF, Deheeger M, Akrout M et al (1995) Influence of macronutrients on
adiposity development: a follow up study of nutrition and growth from 10 months to 8
years of age. International Journal of Obesity Related Metabolic Disorders 19: 573-8.
194. British Paediatric Association (1994) Is breastfeeding beneficial in the UK? Archives of
Disease in Childhood 71: 376-80.
195. Lobstein T & Leach R (2004) Diabetes may be undetected in many children in the UK.
British Medical Journal 328: 1261-2.
196. Owen CG, Martin RM, Whincup PH et al (2006) Does breastfeeding influence the risk of
type 2 diabetes in later life? A quantitative analysis of published evidence. American Journal
of Clinical Nutrition 84: 1043-54.
197. Owen CG, Whincup PH, Gilg JA et al (2003) Effect of breastfeeding in infancy on blood
pressure in later life: systematic review and meta-analysis. British Medical Journal 327:
1189-95.
198. Martin RM, Gunnell D & Davey Smith G (2005) Breastfeeding in infancy and blood pressure
in later life; systematic review and meta-analysis. American Journal of Epidemiology
161: 15-26.
199. Martin RM, Davey Smith G, Mantani P et al (2004) Breastfeeding and cardiovascular
mortality: the Boyd Orr cohort and a systematic review with meta-analysis. European Heart
Journal 25: 778-86.
200. Leeson CP, Kattenhorn M, Deanfield JE et al (2001) Duration of breastfeeding and arterial
distensibility in early adult life: population based study. British Medical Journal 322: 643-7.
201. Owen CG, Whincup PH, Odoki K et al (2002) Infant feeding and blood cholesterol: a study
in adolescents and a systematic review. Pediatrics 110: 597-608.
202. Singhal A, Cole TJ & Fewtrell M (2004) Breastmilk feeding and lipoprotein profile in
adolescents born preterm: follow up of a prospective randomised trial. Lancet 363: 1571-8.
203. Rudnicka AR, Owen CG & Strachan DP (2007) The effect of breastfeeding on
cardiorespiratory risk factors in adult life. Pediatrics 119: 1107-15.
204. Martin RM, Middleton N & Gunnell D (2005) Breast-feeding and cancer; the Boyd Orr
cohort and systematic review with meta-analysis. Journal of the National Cancer Institute
97: 1446-57.
205. Martin RM, Gunnell D, Owen CG et al (2005) Breast-feeding and childhood cancer; a
systematic review with meta-analysis. International Journal of Cancer 117: 1020-31.
206. Greer FR, Sicherer SH, Burks AW et al (2008) Effects of early nutritional interventions on the
development of atopic disease in infants and children: the role of maternal dietary
restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed
formulas. Pediatrics 121: 183-91.
207. Fergusson DM & Woodward LF (1999) Breast feeding and later psychosocial adjustment.
Paediatric & Perinatal Epidemiology 13: 144-57.
208. Montgomery SM, Ehlin A & Sacker A (2006) Breastfeeding and resilience against
psychosocial stress. Archives of Disease in Childhood 91: 990-4.
209. Specker B (2004) Nutrition influences bone development from infancy through toddler
years. Journal of Nutrition 134: 691S-5S.

210. Akobeng AK, Ramanan AV, Buchan I et al (2006) Effect of breastfeeding on risk of coeliac
disease: a systematic review and meta-analysis of observational studies. Archives of Disease
in Childhood 91: 39-43.
211. Singhal A, Cole TJ & Lucas A (2001) Early nutrition in preterm infants and later blood
pressure: two cohorts after randomised trials. Lancet 357: 413-9.
212. Singhal A, Fewtrell M, Cole TJ et al (2003) Low nutrient intake and early growth for later
insulin resistance in adolescents born pre-term. Lancet 361: 1089-97.
213. Singhal A, Cole TJ, Fewtrell M et al (2007) Promotion of faster weight gain in infants born
small for gestational age: is there an adverse effect on later blood pressure? Circulation
115: 213-20.
214. Scaglioni S, Agostoni C, Notaris RD et al (2000) Early macronutrient intake and overweight
at five years of age. International Journal of Obesity Related Metabolic Disorders 24: 777-81.
215. Gunther AL, Remer T, Kroke A et al (2007) Early protein intake and later obesity risk: which
protein sources at which time points throughout infancy and childhood are important for
body mass index and body fat percentage at 7 y of age? American Journal of Clinical
216. Tarini BA, Carroll AE, Sox CM et al (2006) Systematic review of the relationship between
early introduction of solid foods to infants and the development of allergic disease.
Archives of Pediatrics and Adolescent Medicine 160: 502-7.
217. Reilly JJ, Armstron J & Dorosty AR (2005) Early life risk factors for obesity in childhood:
cohort study. British Medical Journal 330: 1357-63.
218. Wilson AC, Forsyth JS, Greene SA et al (1998) Relation of infant diet to childhood health:
seven year follow up of cohort of children in Dundee infant feeding survey. British Medical
Journal 316: 21-5.
219. Niggemann B & Bayer K (2007) Diagnosis of food allergy in children: toward a
standardization of food challenge. Journal of Pediatric Gastroenterology and Nutrition
45: 399-404.
220. Vandenplas Y, Koletzko S, Isolauri E et al (2007) Guidelines for the diagnosis and
management of cows milk protein allergy in infants. Archives of Disease in Childhood
92: 902-8.
221. Osborn DA & Sinn JK (2007) Prebiotics in infants for prevention of allergic disease and food
hypersensitivity. Cochrane Database of Systematic Reviews CD006474.
222. Osborn DA & Sinn JK (2007) Probiotics in infants for prevention of allergic disease and food
hypersensitivity. Cochrane Database of Systematic Reviews CD006475.
223. Fisher DJ, Baird J & Payne L (2006) Are infant size and growth related to burden of disease
in adulthood? A systematic review of literature. International Journal of Epidemiology
35: 1196-210.
224. Horta BL, Barros FC, Victora CG et al (2003) Early and late growth and blood pressure in
adolescence. Journal of Epidemiology and Community Health 57: 226-30.
225. Belfort MB, Rifas-Shiman SL, Rich-Edwards J et al (2007) Size at birth, infant growth and
blood pressure at three years of age. Journal of Pediatrics 151: 670-4.
226. Monteiro POA & Victora CG (2005) Rapid growth in infancy and childhood and obesity in
later life a systematic review. Obesity Reviews 6: 143-54.
227. Baird J, Fisher D, Lucas P et al (2005) Being big or growing fast: systematic review of size
and growth in infancy and later obesity. British Medical Journal 331: 929-31.
228. Stettler N (2007) Nature and strength of epidemiological evidence for origins of childhood
and adulthood obesity in the first year of life. International Journal of Obesity 31: 1035-43.
229. Singhal A & Lanigan J (2007) Breastfeeding, early growth and later obesity. Obesity Reviews
8 (suppl 1): 51-4.

230. Barker DJP, Osmond C, Winter PDW et al (1989) Weight in infancy and death from
ischaemic heart disease. Lancet 2: 577-80.
231. Osmond C, Cooper C, Sayer AA et al (2007) Infant growth and risk of chronic disease in
adult life. Early Human Development 83: S65.
232. Hales CN, Barker DJP, Clark PMS et al (1991) Fetal and infant growth and impaired glucose
tolerance at age 64. British Medical Journal 303: 1019-22.
233. Eriksson JG, Forsen T, Tuomilehto J et al (2003) Early adiposity rebound in childhood and
risk of type 2 diabetes in adult life. Diabetologia 46:190-4.
234. Bhargava SK, Sachdev HPS, Fall CHD et al (2004) Relation of serial changes in childhood
body mass index to impaired glucose tolerance in young adulthood. New England Journal
of Medicine 350: 865-75.
235. Karaolis-Danckert N, Gunther ALB, Kroke A et al (2007) How early dietary factors modify
the effect of rapid weight gain in infancy on subsequent body composition development in
term children whose birth weight was appropriate for gestational age. American Journal of
Clinical Nutrition 86: 1700-8.
236. Sachdev HPS, Fall CHD, Osmond C et al (2005) Anthropometric indicators of body
composition in young adults: relation to size at birth and serial measurements of body mass
index in childhood; the New Delhi birth cohort. American Journal of Clinical Nutrition 82:
456-66.
237. Cooper C, Fall C, Egger P et al (1997) Growth in infancy and bone mass in later life. Annals
of the Rheumatic Diseases 56: 17-21.
238. Victora C, Barros FC, Horta BL et al (2001) Short-term benefits of catch-up growth for
small-for-gestational-age infants. International Journal of Epidemiology 30: 1325-30.
239. World Health Organisation (2004) Global strategy on diet, physical activity and health.
Geneva: World Health Organisation.
240. World Health Organisation (2006) Promoting optimal fetal development: report of a
technical consultation. Geneva: World Health Organisation.
241. Heckman JJ (2007) Economics of health and mortality special feature: the economics,
technology, and neuroscience of human capability formation. Proceedings of the National
Academy of Science USA 104: 13250-5.
242. Shankar AH, Jahari AB & Sebayang SK et al (2008) Effect of maternal multiple
micronutrient supplementation on fetal loss and infant death in Indonesia: a double-blind
cluster-randomised trial. Lancet 371: 215-27.
243. Christian P, Osrin D & Manandhar DS et al (2005) Antenatal micronutrient supplements in
Nepal. Lancet 366: 711-2.
244. Department of Health (1994) Nutritional aspects of cardiovascular disease: report of the
Cardiovascular Review Group, Committee on Medical Aspects of Food Policy. London: The
Stationery Office.
245. Department of Health (1998) Nutritional aspects of the development of cancer: report of
the Working Group on Diet and Cancer of the Committee on Medical Aspects of Food and
Nutrition Policy. London: The Stationery Office.
246. Scientific Advisory Committee on Nutrition (2003) Salt and health. London: The Stationery
Office.
247. Scientific Advisory Committee on Nutrition (2004) Advice on fish consumption: benefits and
risks. London: The Stationery Office.
248. Scientific Advisory Committee on Nutrition (2007) Update on vitamin D. London: The
Stationery Office.
249. Food Standards Agency. The eatwell plate. www.eatwell.gov.uk/healthydiet/eatwellplate
250. Henderson L, Irving K, Gregory J et al (2003) The national diet & nutrition survey: adults
aged 19 to 64 years. Volume 3. London: The Stationery Office.

251. Henderson L, Gregory J & Swan G (2003) The national diet & nutrition survey: adults aged
19 to 64 years. Volume 2. London: The Stationery Office.
252. Scientific Advisory Committee on Nutrition (2006) Folate and disease prevention. London:
The Stationery Office.
253. Kearney JM & McElhone S (1999) Perceived barriers in trying to eat healthier results of a
pan-EU consumer attitudinal survey. British Journal of Nutrition 81: S133-7.
254. Nelson M, Erens B, Bates B et al (2007) Low income diet and nutrition survey. London: The
Stationery Office.
255. Drewnowski A & Specter SE (2004) Poverty and obesity: the role of energy density and
energy costs. American Journal of Clinical Nutrition 79: 6-16.
256. Dinour LM, Bergen D & Yeh MC (2007) The food insecurity-obesity paradox: a review of the
literature and the role food stamps may play. Journal of the American Dietetic Association
107: 1952-61.
257. Wrigley N, Warm D, Margetts B et al (2002). Assessing the impact of improved retail access
on diet in a food desert: a preliminary report. Urban Studies 39: 2061-82.
258. Meiselman HL (2006) The role of context in food choice, food acceptance and food
consumption. In: Shepherd R & Raats M (eds) The psychology of food choice. Oxford: CAB
International.
259. Anderson A (2007) Nutrition interventions in women in low-income groups in the UK.
Proceedings of the Nutrition Society 66: 25-32.
260. Van Teijlingen ER, Wilson BJ, Barry N et al (1998) Effectiveness of interventions to promote
healthy eating in pregnant women and women of childbearing age: a review. London:
Health Education Authority.
261. Fairbank L, OMeara S, Renfrew MJ et al (2000) A systematic review to evaluate the
effectiveness of interventions to promote the initiation of breastfeeding. London: Health
Technology Assessment NHS R&D HTA Programme.
262. Havas S, Anliker J, Damron D et al (1998). Final results of the Maryland WIC 5-a-day
program. American Journal of Public Health 88:1161-7.
263. Arnold CG & Sobal J (2000) Food practices and nutrition knowledge after graduation from
the Expanded Food and Nutrition Education Program (EFNEP). Journal of Nutrition
Education 32: 130-9.
264. Wrieden WL, Anderson AS, Longbottom PJ et al (2007) The impact of community-based
food skills intervention on cooking confidence, food preparation methods and dietary
choices an exploratory trial. Public Health Nutrition 10: 203-11.
265. Ciliska D, Miles E, OBrien MA et al (1999) The effectiveness of community interventions to
increase fruit and vegetable consumption in people four years of age and older. Ontario:
Ontario Ministry of Health.
266. Pomerleau J, Lock K, Knai C et al (2005) Interventions designed to increase adult fruit and
vegetable intake can be effective: a systematic review of literature. Journal of Nutrition
135: 2486-95.
267. Devine CM, Farrell TJ & Hartman R (2005) Sisters in health: experiential program
emphasizing social interaction increases fruit and vegetable intake among low income
adults. Journal of Nutrition Education and Behavior 37:265-70.
268. Dyson L, McCormick F & Renfrew MJ (2005) Interventions for promoting the initiation of
breastfeeding. Cochrane Database of Systematic Reviews CD001688.
269. Britton C, McCormick FM, Renfrew MJ et al (2007) Support for breastfeeding mothers.
Cochrane Database of Systematic Reviews CD001141.
270. Bartington S, Griffiths L, Tate A et al (2006) Are breastfeeding rates higher among mothers
delivering in Baby Friendly accredited maternity units in the UK? International Journal of
Epidemiology 35: 1178-86.

271. Broadfoot M, Britten J & Tappin DM (2005) The Baby Friendly Hospital Initiative and
breastfeeding rates in Scotland. Archives of Disease in Childhood Fetal and Neonatal Edition
90: F114-6.
272. Kramer MS, Chalmers B, Hodnett ED et al (2001) Promotion of breastfeeding intervention
trial (PROBIT). A randomized trial in the Republic of Belarus. Journal of the American
Medical Assocation 285: 413-20.
273. Moore ER, Anderson GC, Bergman N (2007) Early skin-to-skin contact for mothers and
their healthy newborn infants. Cochrane Database of Systematic Reviews CD003519.
274. Hawkins SS, Griffiths LJ, Dezateux C et al (2007) Maternal employment and breast-feeding
initiation: findings from the Millennium Cohort Study. Paediatric & Perinatal Epidemiology
21: 242-7.
275. Abdulwadud OA & Snow ME (2007) Interventions in the workplace to support
breastfeeding for women in employment. Cochrane Database of Systematic Reviews
CD006177.
276. Black MM, Siegel EH, Abel Y et al (2001) Home and videotape intervention delays early
complementary feeding among adolescent mothers. Pediatrics 107: E67.
277. Koehler S, Sichert-Hellert W & Kersting M (2007) Measuring the effects of nutritional
counselling on total infant diet in a randomised controlled intervention trial. Journal of
Pediatric Gastroenterology and Nutrition 45: 106-13.
278. National Institute for Health and Clinical Excellence (2008) Maternal and child nutrition.
London: National Institute for Health and Clinical Excellence.
279. HM Government (2008) Healthy weight, healthy lives: a cross government strategy for
England. London: HM Government.
280. Hills D, Child C, Jungle K et al (2006) Healthy Start: rapid evaluation of early impact on
beneficiaries, health professionals, retailers and contactors. London: Department of Health.
281. Stettler E, Stallings VA, Troxel AB et al (2005) Weight gain in the first week of life and
overweight in adulthood: a cohort study of European American subjects fed infant formula.
Circulation 111: 1897-903.
282. British Medical Association (2005) Preventing childhood obesity. London: British Medical
Association.
283. Government Office for Science (2007) Tackling obesity: future choices outcomes report.
London: Department for Innovation, Universities and Skills.
284. Jablonka E & Lamb MJ (2005) Evolution in four dimensions: genetic, epigenetic, behavioral
and symbolic variation in the history of life. Cambridge: MIT Press.
285. Rassoulzadegan M, Grandjean V, Gounon P et al (2007) Inheritance of an epigenetic
change in the mouse: a new role for RNA. Biochemical Society Transactions 35: 623-5.
286. Laird PW (2005) Cancer epigenetics. Human Molecular Genetics 14: R65-76.
287. Cho E, Willett WC, Colditz GA et al (2007) Dietary choline and betaine and the risk of
distal colorectal adenoma in women. Journal of the National Cancer Institute 99: 1224-31.
288. Godfrey KM, Lillycrop KA, Burdge G et al (2007). Epigenetic mechanisms and the mismatch
concept of the developmental origins of health and disease. Pediatric Research 61: 5R-10R.
289. Li E, Beard C & Jaenisch R (1993) Role for DNA methylation in genomic imprinting. Nature
366: 362-5.
290. Walsh CP, Chaillet JR & Bestor TH (1998) Transcription of IAP endogenous retroviruses is
constrained by cytosine methylation. Nature Genetics 20: 116-7.
291. Waterland RA & Jirtle RL (2003) Transposable elements: targets for early nutritional effects
on epigenetic gene regulation. Molecular and Cellular Biology 23: 5293-300.
292. Bird A (2001) DNA methylation patterns and epigenetic memory. Genes & Development 16: 6.
293. Reik W, Dean W & Walter J (2001) Epigenetic reprogramming in mammalian development.
Science 293: 1089-93.

294. Yoder JA, Soman NS & Verdine GL (1997) DNA (cytosine-5)-methyltransferases in mouse
cells and tissues. Studies with a mechanism-based probe. Journal of Molecular Biology
270: 385-95.
295. www.vegsoc.org
296. www.vegansociety.com
297. Dewey K, Cohen RJ & Rollins NC (2004) WHO technical background paper: feeding of non-
breastfed infants from 6-24 months of age in developing countries. Food and Nutrition
Bulletin 25: 377-402.
298. Williams AF (1998) Infant feeding. In: Campbell AGM, McIntosh N (eds) Forfar and Arneils
textbook of paediatrics. New York: Churchill Livingstone.
299. Behrman RE, Vaughan VC & Nelson WE (eds) (1997) Nelson textbook of pediatrics. 13th
edition. Philadelphia: WB Saunders.
300. Golden BE (2000) Infancy, childhood and adolescence. In: Garrow JS, James WPT & Ralph A
(eds) Human nutrition and dietetics. 10th Edition. Edinburgh: Churchill Livingstone.
301. McCance RA, Widdowson EM, Holland B et al (1991) The composition of foods 5th edition.
London: Royal Society of Chemistry and Ministry of Agriculture, Fisheries and Food.


Index
A
AA see arachidonic acid
adiposity 3, 12, 20
adolescence 28, 42, 46, 50, 61, 63
Adolescent health (2003) ix
advertising 54, 63, 74
AGA see appropriate for gestational age
agriculture 6, 12
albumin 42
alcohol 1, 3, 6, 24, 45, 69
allergic diseases 43, 44-5, 71
ALSPAC see Avon Longitudinal Study of Parents and Children
amino acids 7, 35
analgesics 35
animal models 1, 12, 15, 20, 22, 26, 40
anorexia nervosa 1
antibiotics 35
antidepressants 35
appetite 26, 36, 38, 42, 71, 72
appropriate for gestational age (AGA) 22
arachidonic acid (AA) 41
asthma 13, 43, 44
atopic dermatitis 43, 44, 57
Avon Longitudinal Study of Parents and Children (ALSPAC) 22, 32
B
baby foods see complementary feeding
Baby Friendly Hospital Initiative 1, 57-9, 60
Barker concept see thrifty phenotype hypothesis
basal metabolism 7
Belarus 40, 42, 43, 58
birth weight see also low birth weight
cancer risk 43
disease in adults 16, 18, 19, 21, 42, 43
growth standards 39
maternal dietary supplementation 50-1
maternal obesity and 22
blood pressure
breast feeding and 43, 44
infant weight gain and 45, 48
low birth weight and 15, 16, 19
maternal weight and 21
BMA see British Medical Association
body mass index (BMI)
breast feeding and adult BMI 41, 42
infant weight and adult BMI 16, 17, 22, 45, 48
infant weight and adult disease 46, 47, 48
WHO definition 68

bone mineral content (BMC) 3, 13, 44, 48

brain development 8, 25, 35, 41
breast cancers 43, 45
breast feeding
advantages 26, 40-4
at work 60
blood pressure and 4, 43
bone health and 3, 13, 44, 48
cancers and 43, 45
CHD and 13, 43
coeliac disease 44
cognitive development and 41
confounding 40, 41-2, 42, 43
contraindications 25
CVD and 42
developed countries 40
developing countries 30, 40
diabetes and 42
doctors role 59-60
gastrointestinal diseases and 44
guidelines 27, 34, 71-4
improving initiation and duration 56-60
obesity in adults and 13, 41-2
prevalence 13, 27
reasons for avoidance 28, 29, 38, 56
social class and 5, 27, 30, 41
ten steps to successful breastfeeding 57, 59
weight gain in children 42
weight gain in infants 36, 37, 38
WHO guidelines 34
breast milk 25, 60, 71
contaminants 35
nutrient composition 26, 35, 41, 42, 43, 75
British Medical Association (BMA)
Adolescent health (2003) ix
food labelling statement 64
Growing up in Britain: ensuring a healthy future for our children (1999) ix 13
Improving the health of the worlds poor (2007) 51
Preventing childhood obesity (2005) ix 63
British National Formulary (BNF) 35
bronchitis 43
C
caffeine 32, 35, 36, 69, 71
calcium 44, 52, 69, 70
cancers
breast feeding 35, 43
epigenetic mechanisms 67
infant diet and 13

carbohydrates see also cereals 3

hunter-gatherer diets 5-6
cardiovascular diseases (CVD)
breast feeding and 43
child growth and adult CVD 45-6
developed countries 7-8
developing countries 12
low birth weight and 15
micronutrient feeding in infancy 21, 44
women 46
catch-up infant weight gain 36, 39, 46, 48
cereals see also carbohydrates 6, 44, 53, 72
CHD see coronary heart diseases
child growth
CHD in adults 17, 47
phases 38
chronic diseases 15, 21, 22
mismatch model 9, 10, 11
nutritional transitions 5-7
coeliac disease
infant diet 73
coffee 32, 69, 71
cognitive development
breast feeding 41
infant diet and 13, 45
colostrum 26
Committee on Medical Aspects of Food and Nutrition (COMA) 62
complementary feeding 5, 44
developing countries 25, 34, 36, 51
guidelines 36, 39, 71-2
initiatives 61
UK practice 30-4
conclusions 3-4
confounding 40, 41-2, 42, 43, 58, 60
Cookwell Project 55
coronary heart diseases (CHD)
breast feeding 13, 43
child growth and adult CHD 17, 47
infant and child growth 21
maternal diet and 21
cost benefit analysis 50
cows milk see also dairy food 35, 42, 44, 71, 72, 73

D
dairy food see also cows milk; eggs 44, 53, 69, 70, 72
deoxyribonucleic acid (DNA) 66-7
Department of Health (DH)
alcohol guidelines 69
Good practice and innovation in breastfeeding 26, 34
obesity targets 63
dermatitis 43, 44
developed countries 21
developing countries
breast feeding 5, 30, 34, 40
chronic diseases in 10
complementary feeding 34, 36, 61
infant diet 25, 50-1
maternal diet 21, 35, 50-1
obesity 12-13
developmental origins concept 8-9, 15-19
developmental plasticity 1, 9, 16
diabetes see gestational diabetes; pre-diabetes; type 1 diabetes;
type 2 diabetes
discount model 50
DNA see deoxyribonucleic acid (DNA)
DNA N-methyl transferase (Dnmt) 67
docosahexanoic acid (DHA) 35, 41
doctors role in supporting breastfeeding 59-60
E
Eatwell plate 51, 69
educational attainment
breastfeeding in women and 27, 40, 41, 45
complementary feeding 31, 32, 36
diet in women 53
eggs see also dairy food 6, 42, 44, 69, 72, 73
embryo
environmental effects 19-20
epigenetic mechanisms 20-1
energy
balance with nutrition 10-11
density/cost of food 54, 72
food sources 6, 7
England
infant mortality 25
obesity 11
epigenetic mechanisms 10, 11, 20-1, 66-7
European Childhood Obesity Project 40
evolution 5-6, 10
exercise 3, 6, 50
Expanded Food and Nutrition Education Programme (EFNEP) 55

F
families
attitudes to breast feeding 28
influence on food choice 2, 54, 55, 56, 62
feeding behaviour
infant 26, 32, 36
maternal 53-4
fetal growth
breast milk and 26
hormones 38
menarche and 50
fetal nutrition 15-24
fetal origins concept 21
fetal programming 16
fetal supply mechanisms 19-20
finger foods 72
fish see also seafood 34, 44, 51, 54
fizzy drinks 32, 53, 71
folate deficiency 5, 20, 21, 52, 67, 68
food choice see feeding behaviour
food labelling 64
food safety 73
food security 12, 53-4
food skills 55, 56
Food Standards Agency (FSA)
infant feeding guidelines 71-4
maternal diet guidelines 34-5, 64
Foresight Project, Tackling obesities: future choices 63
formula milk
advertising 35, 74
composition 35-6
guidelines 71-4
long-term outcomes 44
neurodevelopment 41
nutrient composition 75
weight gain in infants 36, 37, 38
fruit
consumption by infants 32, 71, 72
consumption by women 51, 52, 53-4, 56, 69
Healthy Start scheme 62

G
galactosaemia 35
Gambia 50-1
gastrointestinal tract 8, 36
breastfeeding and 34, 40, 57
Gateshead Millennium Baby Study (1999-2000) 27
general practitioners (GPs), breastfeeding policy 59-60
gestational diabetes 12, 22, 36
Global strategy on diet, physical therapy and health 50
gluten 44, 73
glycaemic index 3, 22, 23
glycine insufficiency 7
goats milk 71
goitre 6
Good practice and innovation in breastfeeding 26, 34
grains see cereals
Growing up in Britain: ensuring a healthy future for our children (1999) ix 1-2, 13
Growth Acceleration Hypothesis 45
growth hormones 38
Guatemala 21, 44
H
Healthy Start scheme 2, 36, 62
heart diseases see coronary heart diseases (CHD)
heart muscle cells 9
high-density lipids (HDL) 21, 44, 45
HIV 35, 50, 71
honey 6, 31, 73
hypertension 9, 12, 15, 22, 51
I
IFS see under infant feeding
immunity 7, 13
INCAP see Institute of Nutrition of Central America and Panama
income, diet in women 53-6
India 21
inequalities in health 13, 61-2
infant diet 13, 25-49
adult obesity and 13, 16, 63
effect of maternal diet 32-3, 33
global perspective 50-1
guidelines 27, 71-4
long-term outcomes 43-9
pre-term infants 44
vitamin supplements 36

infant feeding
appetite 26, 36, 42
behaviour 32, 33, 36, 73
Infant feeding survey (2005) 3, 27, 30, 31
infant growth
adult health and 17, 45-8
charts 38-9
determinants 36-9
height and adult CVD 47
infant mortality 25, 40
infant weight
determinants 36-9
health in adults 12, 15-19, 22, 46
optimal gain 48, 49
rapid gain 13, 48
Repositioning nutrition as central to development 50
waist circumference in adults 12
inflammatory bowel diseases 44
Institute of Nutrition of Central America and Panama (INCAP) 21, 44
insulin
infant growth and 21, 38
low birth weight and 15, 19
intelligence quotient (IQ) 41
intrauterine growth restriction (IUGR) 16, 36
iodine 6, 35, 70, 75
ischaemic heart diseases see coronary heart diseases
J
Japan 22
L
large for gestational age (LGA) 22
leptin 20, 26
long-chain polyunsaturated fatty acids (LCPUFAs) 7, 70
brain development 41
in breast milk 26, 35
low birth weight see also birth weight
health in adults 15-19
waist circumference in adults 12
Low income diet and nutrition survey 53-4

M
maternal diet
CHD in adults 21
diabetes in adults 21
effect on fetus 19-20, 21
effect on infant diet 32-3, 33
food choice 53-4
global perspective 50-1
guidelines during lactation 34-5
guidelines during pregnancy 69-70
improvement interventions 55-6
obesity in adults 12
WHO report 50
maternal obesity
birth weight and 22
fetal adiposity and 12
maternal-child relations 41
meat see protein
menarche 50
mental health, breast feeding and 43, 60
metabolic integrity 7
metabolic syndrome 20
micronutrients
for mothers 34, 51
in obesity 5
supplements in infants 44
vegetarianism and veganism 70
middle classes see social class
migrants 10
milk see breast milk; cows milk
Millennium Cohort Study 58, 60
mismatch model 9, 10, 11, 16
mortality 6
infant 25, 40
muscle growth 8, 13
N
National Diet and Nutrition Survey (NDNS) 51-2
National Institute for Health and Clinical Excellence (NICE)
guidance on breastfeeding 34, 60
nutritional policy 62
Netherlands 21
neurodevelopment 35, 41
NICE see National Institute for Health and Clinical Excellence
Northern Ireland 11
Norway 15, 19
nucleotides 35-6

nutrition
inequalities 61-2
plane 18
what is good nutrition? 7
nuts 6, 31, 34, 44, 72, 73
O
obesity
developing countries 12-13
European Childhood Obesity Project 40
infant birth weight and 16
intervention programmes 63
prevalence 11, 12
UK government strategy 63, 64
WHO definition 68
oestrogen 38
oligosaccharides 26, 35-6, 45
optimal infant weight gain 48, 49
otitis media 40
ovarian cancers 34
overnutrition 5, 13, 18, 20
P
paediatricians, breastfeeding policy 59-60
pancreas 8, 9, 42
peanuts 34, 73
physical activity see exercise
plasticity 1, 9, 16
pre-diabetes 42
pre-formed nucleotides 35-6
pre-term infants 16, 35, 36, 39, 40, 41, 44, 45
prebiotics 35-6, 45
pregnancy, dietary guidelines 69-70
Preventing childhood obesity (2005) ix 63
probiotics 45
professional classes see social class
Promoting optimal fetal development 50
protein
allergy and 44
consumption by women 69
in eggs 42
in formula milk 38, 44
prudent diet 32, 33, 53
psychotropic drugs 35
puberty 38
Pune Maternal Nutrition Study 21

R
rapid infant weight gain 13, 48
respiratory infections, breastfeeding and 34, 40
retinal development 41
rickets 6
Royal College of Paediatrics and Child Health (RCPCH) 39
S
salt 6, 31, 51, 73
Scientific Advisory Committee on Nutrition (SACN) 34, 39
Scotland
Baby Friendly Hospitals survey 58
birth weight and CHD 18-19
breast feeding initiation project 57
Cookwell Project 55
obesity 11
seafood see also fish 69
allergy and 44
separation of mother from infant 60
sex factors 36, 37
shops 54
skin-to-skin contact 60
small-for-gestational-age (SGA) infants 36, 44
smoking 32, 35
social class
breast feeding 5, 27, 30
complementary feeding 31-2
diet in women 53
infant mortality 25
solid foods see complementary feeding
Southampton Womens Survey 22, 32, 53
soya 43, 44, 71
Special Supplemental Nutrition Programme for Women,
Infants and Children (WIC) 55, 61
stroke 12, 13, 19-20, 45
sugars 6, 20, 32, 51, 53, 61, 69, 71, 73
sunlight 36
Sure Start 62
Sweden 19
T
Tackling obesities: future choices 63
taurine 35, 75
tea 32, 71
testosterone 38
thrifty phenotype hypothesis 8, 9
thyroid hormones 38

timing of introducing foods 31, 44-5

trainer cups 32
transgenerational effects 22-3
tuberculosis 35
type 1 diabetes
breast feeding 42
in children of mothers with gestational diabetes 22
type 2 diabetes
developed countries 7-8, 12
developing countries 12, 21, 22, 42, 46
fetal development and 8, 12
obesity and 42
U
UK Gateshead Millennium Baby Study 27
United Nations, Millennium development goals 51
United States
diet 6
nutritional intervention programmes 55, 56, 61
unpasteurised foods 69
V
vegetables
consumption by women 51, 53-4, 61, 69, 72
consumption intervention programmes 55-6, 64
in diet 6, 51-2
Healthy Start scheme 62
infant diet 27, 32, 36, 44, 72
vegetarianism and veganism 70, 72
vitamin A
infant diet 72
supplements 36, 69
vitamin B 7, 21, 35, 70
vitamin D
deficiency 5, 69
infant diet 32
maternal diet 51
supplements 34, 36, 69
vegetarianism and veganism 70
vitamin supplements
infants 36, 73
maternal to improve fetal development 50-1, 69

W
Wales
infant mortality 25
obesity 11
water (drinking) 71
weaning see complementary feeding
Welfare Foods scheme 62
women
breastfeeding initiatives 56-60
complementary feeding initiatives 61
CVD in 46
guidelines to improve diet 51-2
nutrition intervention programmes 55-6
work 32, 60
working classes see social class
World Bank, Repositioning nutrition as central to development 50
World Health Organization
BMI definition 68
breast milk substitutes marketing guidelines 74
breastfeeding guidelines 34
Global strategy on diet, physical therapy and health 50
infant feeding guidelines 71-4
infant growth charts 38-9
Promoting optimal fetal development 50
World Health Organization/UNICEF
Baby Friendly Hospital Initiative 57-9
doctors role 59-60
NICE recommendations 60
Y
young people 1, 51-2
Z
zinc 7, 52, 75

The BMA is committed to protecting the environment by
using papers that contain a high percentage of recycled fibre
or those approved by the Forestry Stewardship Council (FSC)
label that guarantees the harvested trees are replaced or are
allowed to regenerate naturally. When you have finished
with this publication, please recycle it responsibly.
CODE: BMA 49484 /AB / SCIENCE & EDUCATION/ 02.09
BMA Board of Science, British Medical Association, BMA House, Tavistock Square, London, WC1H 9JP
www.bma.org.uk
British Medical Association, 2009



Early Life Nutrition and Lifelong Health PDF

Hochgeladen von

Dokumentinformationen

Originaltitel

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Early Life Nutrition and Lifelong Health PDF

Hochgeladen von

Copyright:

Verfügbare Formate

BMA Board of Science

Early life nutrition and

Early life nutrition and

Early life nutrition and lifelong health i

Chair, Board of Science Professor Sir Charles George

Director of Professional Activities Professor Vivienne Nathanson

Head of Science and Education/Project lead Nicky Jayesinghe

Authors Professor Mark Hanson

Contributors Luke Garland

Editorial secretariat Thom Ellinas

Indexer Richard Jones

British Library Cataloguing-in-Publication Data.

Cover photograph: Getty Images

ii Early life nutrition and lifelong health

Sir Kenneth Calman President, BMA

Early life nutrition and lifelong health iii

Professor Mark Hanson, Director Institute of Developmental Sciences, Director Developmental

Address for correspondence: Professor Mark Hanson, Institute of Developmental Sciences,

iv Early life nutrition and lifelong health

About the authors

Early life nutrition and lifelong health v

vi Early life nutrition and lifelong health

Adiposity relating to, or composed of adipose tissue containing fat cells

Early life nutrition and lifelong health vii

viii Early life nutrition and lifelong health

Professor Sir Charles George

Early life nutrition and lifelong health ix

x Early life nutrition and lifelong health

List of figures xiii

Chapter 1: The importance of fetal and infant nutrition 5

Chapter 2: Fetal nutrition: impact on development and later life 15

Chapter 3: Infant nutrition 25

Early life nutrition and lifelong health xi

Breastfeeding and health: short- and long-term outcomes 40

Chapter 4: Influences on maternal and infant nutrition and

Appendix 1: Epigenetic processes 66

Appendix 2: Definition of overweight 68

Appendix 3: Current UK dietary recommendations for pregnancy 69

Appendix 4: Infant feeding guidelines 71

Appendix 5: The International Code on the Marketing of Breast Milk Substitutes 74

Appendix 6: Comparison of the nutrient composition of mature

xii Early life nutrition and lifelong health

Figure 1: The human dietary transition 6

Early life nutrition and lifelong health xiii

xiv Early life nutrition and lifelong health

Early life nutrition and lifelong health 1

2 Early life nutrition and lifelong health

Early life nutrition and lifelong health 3

4 Early life nutrition and lifelong health

Chapter 1: The importance of fetal

Nutritional transitions and patterns of chronic disease

Early life nutrition and lifelong health 5

Figure 1: The human dietary transition

Hunter-gatherer energy sources USA energy sources

65% Fruits 17%

A typical hunter-gatherer diet versus a typical modern USA diet.

6 Early life nutrition and lifelong health

What is good nutrition?

The developmental consequences of inappropriate nutrition

Early life nutrition and lifelong health 7

The importance of development for later health

8 Early life nutrition and lifelong health

Figure 2: The thrifty phenotype hypothesis